cz

food news

radios

ViroLIEgy

ViroLIEgy
12 Aug 2022 | 4:16 pm

Getting the Monkey(pox) off the Back With Patrick Timpone


A few days ago, I had the honor of being a guest on the Patrick Timpone show for the third time. As usual, the conversation was entertaining, even beyond the fact that I unknowingly wore the exact same shirt as when I was on the show a few months ago. We covered many topics in our hour long chat which was nicely listed in order on Patrick's site:

How Can Monkey Pox Exist If the Germ Theory Is False?

Mike did video with Dr. Cowan about monkeypox.  It's on ViroLIEgy.com.  Many articles there.

Monkeypox is more of the same.  Nonspecific symptoms, unusual presentations, usually in genital areas, a targeted victim group, victims pegged with a faulty PCR test while presenting for other symptoms.

Monkeypox confused with herpes.  Friction, sweat, stress, anxiety, immune-suppressing drugs will cause the lesions.  Thin skin, lack of collagen related to herpes.

Had a drill before monkeypox outbreak similar to Event 201. 

Initial victims had no travel or contact with anyone from the monkeypox endemic areas such as Africa.

Dr. Luc Montagnier said they never purified a virus. 

AZT causes same symptoms as HIV/AIDs.  Very toxic.  Was a failed chemo drug in the 70s. 

Contagion is a myth.  Studies trying to transmit 1918 Flu couldn't.  Measles parties shown not to transmit measles to all exposed.

Epidemiological studies are subjective and often biased.  Need to look at patient's environment.  

Bioresonance possibly explains "catching" a virus.

Virologists believe it.  They don't question because they have a lot invested in their education and position.  We're taught not to look at outside factors or to question the establishment. 

Look at the information for yourself.  They're going to keep playing the same trick over and over again. 

Culturing by putting in lots of other toxic substances that break down the cells, then isolating and saying it's a virus.

7 main "coronavirus" now, and they all look the same.  In a study, spikes created by a procedure that eroded the cell membrane.  Can't see a "live virus" in an electron microscope, it must be killed first.  Which alters it and creates artifacts.

Can bioweapons be created?  99% of people survived COVID – it was a poor bioweapon.  The real bioweapon is the jab.  All they needed was the fear to induce people to get it.  They can poison us though, and they are.

Gain of function – another fiction. 

Shedding from the jab – another fear campaign. 

Are viruses racist and homophobic?  Those are identified as the target groups.

See the No Virus Challenge on viroliegy.com.  Also see Debunking the Nonsense.

You can watch our discussion here:

I hope that you are able to come away with some useful information!

ViroLIEgy
8 Aug 2022 | 3:33 pm

Rabies: The “Virus” of Fear


While walking down the darkened street late at night, have you ever had that gnawing fear as to whether or not the posse of raccoons rummaging through the trashcans nearby, staring at you with their beady yellow eyes, are ready and waiting for the right moment to pounce? Or have you ever had your fingertip accidentally pierced by the sharp fangs of a squirrel while feeding it walnuts and had to rush to the hospital on a nurses advice only to be told by the doctor that squirrels do not carry the "deadly virus?" Have you ever been bit in the very tender thin space of skin in between your thumb and index finger by a baby penguin while feeding it fish at the Omaha Zoo?  Ok, the last one is obviously not related to rabies as the "virus" discriminates as to which animals it infects. Whether or not the squirrel can get or transmit rabies depends upon who you ask. In any case, these are all true experiences for me and yes, I have been bitten by numerous animals while feeding them. Like many, I have encountered the fear of being infected by a bite from a potentially rabid animal and that if I waited too long to receive treatment, it would be too late to stop the "virus" before it invades my cerebral cortex and causes me to turn into a crazed barking dog-man. Fortunately, not one of my comedically unfortunate puncture wounds left me to succumb to any disease. As I would later find out, my fears were in fact as irrational as the myths surrounding rabies which are built upon a foundation of fraud and pseudoscience.

Still, rabies seems to be one of the diseases that those who cling to the "virus" narrative love to bring up as if it is the Holy Grail of proof that "viruses" actually exist. Over the decades, the images of the mangy frothing dog snarling and ready to attack has been deeply ingrained into our subconscious through effective media fear-based propaganda.

A mad dog on the run in a London street: citizens attack it as it approaches a woman who has fallen over. Coloured etching by T.L. Busby, 1826. Wellcome Library, London.
1870's fear propaganda.
Atticus Finch taking aim to put down a rabid dog in 1962's To Kill A Mockingbird.
Stephen King's Cujo – striking fear into the impressionable minds of viewers in the early 1980's.

The portrayal of angry diseased animals heightened peoples fear of anything wild and undomesticated and created in their minds the living walking embodiment of an invisible "virus" coming to infect the defenseless with a slobbery bite. The fear of aquiring the deadly disease was the perfect tool to use by Louis Pasteur in the late 1800's to ensare people into the emerging germ theory narrative. All it takes is one bite for the sneaky "virus" to find its way into the bloodstream, attacking the brain and causing a painful death. It seems, upon first glance, to be an open and shut case. However, what you will find upon researching rabies is that the presented model of the rabid animal bite transferring an infectious "virus," which in turn causes disease, is not an accurate portrayal whatsoever and was merely a frightening myth used to propagate the delusions of a madman looking to aquire fame, fortune, and prestige.

A few months ago, I looked at the unethical and fraudulent practices Louis Pasteur employed in the 1880's in his attempt to prove a rabies pathogen exists and causes disease in order to sell his vaccines. Pasteur openly admitted to not being able to isolate any microorganism said to cause rabies but developed his vaccine against the invisible pathogen anyways. This is also openly admitted as well by the Institut Pasteur:

"Louis Pasteur's initial efforts to isolate the rabies virus proved unsuccessful as the virus remained invisible. Viruses could not be seen due to the poor resolution of the microscopes used. The virus was not seen until almost a century later, in 1962, with the advent of electron microscopy.

But as rabies is a disease of the nervous system, together with Emile Roux, Louis Pasteur then had the idea of inoculating part of a rabid dog's brain directly into another dog's brain. The inoculated dog subsequently died."

https://www.pasteur.fr/en/institut-pasteur/history/troisieme-epoque-1877-1887

Thus, Pasteur never worked with any purified and isolated "virus" and did what virologists still do today, which is assume an invisible entity is floating freely in the unpurified solutions of diseased animals which are then inoculated into healthy animals in attempts to cause disease and prove pathogenicity. Interestingly, as stated in the 1930 paper below, Pasteur would fail many times in his attempts to infect animals with saliva from animals claimed to be rabid, the very fluids the "virus" is supposed to reside in. Even if deemed successful, the symptoms would not appear for months, which was unheard of for any pathogen. Thus, he sought other means of infecting animals by way of injecting dogs directly in the brain with the emulsified cranial goo from animals claimed to be rabid. Once the healthy animal died from the toxic brain injection, this was considered a success:

Pasteur's Work with Rabies

"Inoculation with saliva was found to be a method which did not always produce rabies and symptoms did not declare themselves for months. The theory that the disease virus attacks the nerve centers had already been set forth by Dr. Dubous of Paris. Pasteur accordingly inoculated a number of animals subcutaneously with some of the brain substance from other animals which had died of rabies. Most of those inoculated developed rabies, but not all.

Pasteur then conceived the idea of introducing into the brain of experimental animals some of the nerve tissue from an animal which had died of rabies. This experiment was based on the principle of providing the causal organisms with the nutritive medium best suited to their requirements. Pasteur, obliged to sacrifice so many animals, had a real dislike for vivisection; if the animal cried out a little he was full of pity. The idea of perforating the skull of the dog was repulsive to him, he wanted it done but dreaded seeing it done. So it was done one day when he was away. The next day when he was told of the intra-cranial inoculation he was moved to pity for the poor dog."

https://doi.org/10.2307/3410286

While the exact make-up of the inoculations remain a mystery due to Pasteur's secretive nature, the vaccine's he utilized contained a neurotropic agent which was known to cause the exact same neurological conditions as seen in rabid animals. While injecting anything into the brain would potentially cause neurological damage and death, it is not far fetched to believe Pasteur used the same neurotropic agents in his experimental inoculations to prove pathogenicity, especially as they were said to consist of emulsified brain and nervous tissue. This created an issue in determining whether it was the invisible "virus" or the injections themselves which caused neurological damage and/or death. However, it has been admitted that the vaccines themselves led to the majority of neurological conditions rather than "wild" rabies cases as this was considered a rare occurrence in nature. This is just another in a long history of cases where the vaccine created the disease it was supposed to be preventing.

Fortunately, we can learn a lot of interesting tidbits about rabies (or the lack thereof) from the work of Gerald Geison, a leading Louis Pasteur researcher and historian who was privy to his private notebooks. In a 1978 essay he wrote on the ethics of rabies vaccination, Geison pointed out some of the pecularities of rabies such as the fact that it has always been considered a rare disease in man as well as the fact that rabies can not be transmitted from person-to-person. He also noted that, as a pathogenic disease, rabies has an unusually long incubation period. While it is said to usually last 6 to 8 weeks, Geison claimed that it can actually last for a year or more. In fact, there have been reported cases with a rabies incubation period from 6 years all the way on up to 25 years. If that wasn't outlandish enough to make one question the validity of what we are told of the disease, Geison stated that there was a high degree of uncertainty regarding the correlation between animal bites and rabies symptoms as well as the threat of death from being bitten by a clearly rabid animal:

Pasteur's Work on Rabies: Reexamining the Ethical Issues

"Rabies has always been rare in man. It probably never claimed more than a hundred victims in any year in France, and Fiench estimates for the years immediately preceding Pasteur's famous work indicate an annual mortality of considerably less than fifty. In addition, rabies is not an infectious disease in the usual sense; it is not transmitted from man to man. Because of these two features, general or compulsory vaccination has never seemed appropriate with respect to rabies. 

"An even more peculiar feature of rabies is its long incubation period in the absence of detectable symptoms. No other lethal disease of rapid clinical course even approaches rabies for length of incubation-usually six to eight weeks, but sometimes a year or more.

"Unfortunately for Pasteur and his successors, there is a very high degree of uncertainty in the correlation between animal bites and the subsequent appearance of rabies-even when the biting animal is certifiably rabid. While the mortality of clinical rabies is virtually 100 percent, the threat of death from the bite of a rabid animal is vastly less. The risk depends on several factors, including the species of attacking animal (wolf and cat bites, for example, pose a much higher risk than dog bites), the location and depth of the bites, and the application or timing of cauterization. Depending on these and other circumstances, estimates of the risk of contracting rabies from the bites of animals known to be rabid range from as high as 80 percent to as low as 0.5 percent. It is perhaps futile to try to settle upon a meaningful "average" figure within this range, but Pasteur himself estimated that 16 percent of those bitten by rabid dogs would eventually die of rabies unless they submitted to his new treatment."

In his 1995 book The Private Science of Louis Pasteur, Geison pointed out that, according to the English Commission on Rabies, there was also much uncertainty in the rabies statistics. They had suspected that at least one man had died not from rabies but from Pasteur's vaccine instead and they actually favored animal regulations over Pasteur's vaccination approach:

"But the English commission also drew attention to the uncertainty of all statistics on rabies, citing the difficulty of establishing that the attacking animal had in fact been rabid as well as the variable effects of the location and depth of bites, of differences in the lethality of rabid animal bites in different species and races, and of the possible prophylactic effects of cauterization or other treatments applied to bitten victims before they submitted to Pasteur's treatment. The commission also suspected that at least one man may have died as a direct result of the Pastorian injections, and in the end it favored strict regulations on potentially rabid animals (muzzling and quarantine) over Pasteur's more drastic remedy."

We also find out from Geison that, in great contrast to what we are told about rabies, the great majority of rabies victims could forgo any treatment and never have any ill effects whatsoever:

"In short, the great majority of the victims of rabid animal bites could forgo Pasteur's treatment without experiencing any untoward consequences in the future. And they had to decide whether or not to submit to the treatment at a point when they had no symptoms of the disease. For the efficacy and very possibility of Pasteur's vaccine depended on the peculiarly long incubation period that separates the infective bites of a rabid animal from the outbreak of symptoms."

Geison even spotlighted what was known as "false rabies," which were cases of the exact same symptoms of disease associated with rabies that occured despite a complete lack of the victim being bitten by a rabid animal. These symptoms were said to be either induced solely based on fear alone or by alcoholism. In other words, just the mere thought of rabies could create an intense enough reaction inducing the same disease, thus no invisible microscopic pathogen is necessary. Pasteur actually emphasized these cases in defense of his vaccine as there was a growing chorus of criticism that his vaccine did not protect the victims and in fact induced the symptoms of rabies which lead to their deaths. Pasteur therefore had a vested interest in showing that these same symptoms could occur outside of animal bites and vaccination:

"Pasteur himself later pointed out some of the uncertainties surrounding the diagnosis of rabies. Two years after I'affair Girard, for example, he spoke to the Academie des sciences about several cases of "false rabies." Relying on the authority of one Dr Trousseau, Pasteur cited two cases in which symptoms of the disease had been induced solely by fear. In one case, a man suddenly displayed several of the classic features of rabies—including throat spasms, chest pain, extreme anxiety, and other nervous symptoms—merely because the disease had become the subject of a lunchtime conversation. And this man had never even confronted a rabid animal. Presumably more common was the second case, that of a magistrate whose hand had long before been licked by a dog later suspected of rabies. Upon learning that several animals bitten by this dog had died of rabies, the magistrate became extremely agitated, even delirious, and displayed a horror of water. His symptoms disappeared ten days later, when his physician persuaded him that he would already be dead had he been afflicted with true rabies."

In this same address, Pasteur commented upon a recently published case history of "false rabies." Partly because it includes an arresting account of the classic symptoms of rabies, his commentary deserves quoting at length. As recorded in the Comptes rendus of the Academie des sciences for 17 October 1887, Pasteur spoke as follows:

The patient to whom Mesnet refers in his brochure was an alcoholic who, having seen some sort of deposit m his glass during lunch, was seized by a feeling of horror toward the liquid and by a constriction of the throat, followed by headache and by lameness and fatigue in all his limbs. He spent Sunday in this state.

During that night and during the day on Monday and Tuesday, no sleep, a fit of suffocation, throat spasms, and a horror of liquids, which he pushed aside in his glass. His countenance expressed disquiet. His eyes were fixed, glazed, the pupils greatly dilated. His speech was brief, jerky, rapid. He had difficulty breathing. When he was offered a glass of water, he pushed it aside with terror, and suffered fits of suffocation and of constriction of the throat. Bright objects and light were particularly disagreeable to him. He was painfully affected when the air was agitated in front of his face. He died Wednesday night after having suffered from a violent delirium, with extreme agitation, howls and cries, extremely abundant salivation, spitting, biting his bedsheets, and trying also to bite the person taking care of him. In short, this man displayed all the features of furious rabies [I'hydrophobie funeuse]. But he did not die of rabies. He had never been bitten and on several occasions, at long intervals, had already displayed symptoms analogous to false rabies. This man was an alcoholic and belonged, moreover, to a family m which one member had died of insanity [alienation mentale].

By October 1887, when he gave this address, Pasteur had a vested interest in emphasizing the difficulty of diagnosing rabies. For he was then defending himself against allegations that his rabies vaccine not only sometimes failed to protect those who submitted to it, but in some cases was itself the cause of rabies and therefore death. A few hostile critics were insisting that some people died of rabies not only despite Pasteur's vaccine but because of it, and they tried to make Pasteur and his treatment responsible for the
death of anyone who displayed any symptoms of nervous disease. In defense of his vaccine, Pasteur now emphasized the extent to which symptoms like those of rabies could appear in patients who did not have the disease. He therefore insisted that a diagnosis of rabies could only be established with confidence by experiments in which tissue from the victim's brain was transmitted to animals susceptible to the disease."

https://www.jstor.org/stable/j.ctt7zv2b1

"Fake" hydrophobia = one of the defining rabies symptoms can be explained by the generation of fear

There is good reason for the high degree of uncertainty over the correlation between animal bites and the development of symptoms, the actual rabies statistics, as well as the ability to accurately diagnose the disease. For starters, there are many other conditions that can cause the exact same symptoms as rabies in both animals and in humans. In animals, canine distemper, encephalitis, and poisoning are a few of the conditions which can mimic rabies. In humans, this includes polio, being drunk and/or intoxicated on certain drugs, having Guillain–Barré syndrome, and as stated previously, encephalitis derived from the toxic vaccine itself.

It has been stated that it is common not to even find bite marks in cases of rabies and often, the person has had no idea that they were ever bitten to begin with. One source stated that fewer than one third of human rabies victims show evidence of bite wounds. With the vast range of conditions that mimic rabies and the lack of bite marks, it's safe to question the existence of a specific disease known as rabies. It would be logical to conclude that rabies is nothing but the same set of symptoms that has been given a different label numerous times.

This uncertainty in rabies cases and statistics boils down to the inability to accurately diagnose a rabies case. For much of the 1800s to the mid 1900s, rabies was diagnosed upon clinical symptoms which, as previously stated, were not specific to the disease. It is also noted in the WHO's rabies laboratory manual that the histological diagnosis for rabies, which began in the late 1800's, was also non-specific:

Excerpt from the WHO's Laboratory Techniques in Rabies

When factoring in the non-specificity in diagnosis, the uncertainty in the correlation between animal bites and disease symptoms, and the vast majority of victims never needing any treatment whatsoever, it leads one to conclude that the rabies myth is vastly overstated. It is fictitious fear propaganda rather than facts based in reality. We can break this deception down even further by looking at how rabies is diagnosed in the present versus how it was in the past. According to the CDC:

Diagnosis in animals

"A diagnosis of rabies can be made after detection of rabies virus from any part of the affected brain, but in order to rule out rabies, the test must include tissue from at least two locations in the brain, preferably the brain stem and cerebellum.

The test requires that the animal be euthanized. The test itself takes about 2 hours, but it takes time to remove the brain samples from an animal suspected of having rabies and to ship these samples to a state public health or veterinary diagnostic laboratory for diagnosis."

https://www.cdc.gov/rabies/diagnosis/animals-humans.html

In order to diagnose rabies, the animal must be killed and sections must be taken from the brain in order to try and detect the "virus." We already have a few problems here as no "virus" was ever purified and isolated in order to determine how to detect it. There is also an issue with attempting to determine anything from dead tissue as the tissue, once removed, immediately starts to change through decomposition. Biologist Harold Hillman often pointed out the faults in trying to establish credible information about what occurs inside living beings from the study of dead tissues:

"Killing an animal changes its biochemistry grossly. For example, its blood carbon dioxide, phosphate, lactate, and potassium ion concentrations, rise, while its oxygen, sodium ion, adenosine triphosphate, phosphocreatine, concentrations go down. These changes affect much of the tissue metabolism. It is hoped and normally assumed that they will reverse during incubation. There is no realistic way of testing this, since the volume and chemistry of the tissue changes during incubation. In this circumstance, it is worth asking whether cell biologists should use tissues in vitro at all. Perhaps, they should confine their experiments to working on intact animals and human beings, tissue cultures, unicellular organisms and plants."

Click to access a-radical-reassessment-of-the-real-cellular-structure-of-the-mammalian-nervous-system.pdf

The current "gold standard" used to study the dead brain tissue for the diagnosis of rabies is known as the direct fluorescent antibody test. As the name implies, the test looks to detect rabies antigens on the brain by using antibodies said to be specific to the rabies "virus:"

Direct Fluorescent Antibody Test

"The dFA test is based on the observation that animals infected by rabies virus have rabies virus proteins (antigen) present in their tissues. Because rabies is present in nervous tissue (and not blood like many other viruses), the ideal tissue to test for rabies antigen is brain. The most important part of a dFA test is flouresecently-labeled anti-rabies antibody. When labeled antibody is incubated with rabies-suspect brain tissue, it will bind to rabies antigen. Unbound antibody can be washed away and areas where antigen is present can be visualized as fluorescent-apple-green areas using a fluorescence microscope. If rabies virus is absent there will be no staining."

https://www.cdc.gov/rabies/diagnosis/direct_fluorescent_antibody.html

According to the CDC, in the 50 years that the dFA test has been used to detect rabies, it has not failed to present reliable and accurate results. This indirect method is somehow said to be more sensitive and specific than actually "isolating" the "virus," thus the "gold standard" label. It is also stated by the CDC that the saliva of an infected animal contains millions of "virions," making the lack of any purified and isolated "virus" and the reliance on indirect antibody testing all the more glaring of an issue:

Accuracy of the Tests

"During the 50 years the direct fluorescent antibody (DFA) test has been used in the United States, there has been no indication it has failed to provide accurate clinical information on the rabies status of an animal for the purposes of treating an exposed person.

Because of its high sensitivity and specificity, in comparison to virus isolation methods, the DFA test is the "gold standard" diagnostic method for rabies and has been rigorously evaluated by international, national, and state health laboratories. The DFA test is currently the only recommended diagnostic method for routine rabies determination in animals in the United States.

During clinical disease, millions of viral particles may be found intermittently in the saliva. In theory, only a single rabies particle or virion is required to result in a productive infection."

https://www.cdc.gov/rabies/diagnosis/accuracy.html

Returning to the WHO's rabies manual, it shows us exactly how the dFA is used and how the diagnosis is determined based on the interpretation of the person reading the results. The interpreter uses an antigen fluorescence intensity and distribution scale from +4 on down to +1 to determine one of four conclusions: positive, negative, unsatisfactory, or inconclusive. Obviously, the subjective bias of the interpreter plays no role in the accuracy of the determination as humans rarely make interpretive errors, correct?:

From the WHO's Laboratory Techniques in Rabies:

https://www.google.com/url?sa=t&source=web&rct=j&url=https://apps.who.int/iris/bitstream/handle/10665/310836/9789241515153-eng.pdf&ved=2ahUKEwiliY6S66_5AhX5jokEHb2GCT84ChAWegQICxAB&usg=AOvVaw12GvHufua9bB36MzV5Q1xR

In fact, there are many drawbacks to using the dFA as the "gold standard" test for rabies diagnosis beyond the aforementioned use of dead tissues. For starters, due to the lack of ever properly purifying and isolating the rabies "virus" directly from the saliva said to contain millions of "virions," any antibody result is utterly meaningless as there is no "virus" to determine a specific reaction with. We also have this same purification/isolaton problem with antibodies as these entities have also never been taken and separated directly from the fluids of a host in order to be studied independently. There is also the issue that the theoretical antibodies themselves are entirely non-specific and are regularly said to bind to proteins that are not the intended target. Thus, we once again run into the problem where one fictional entity (the rabies "virus") is said to be detected by another fictional entity (the antibody). It is very telling that the CDC believes that the interpretive results from this indirect circular test is more accurate than actually finding and "isolating" the supposed "virus."

Thus, we must ask ourselves if these dFA tests really are as accurate as stated by the CDC. If we do so, we find out that this is most definitely not the case according to these next three sources. This first snippet comes from a study done on bacteria which points out the obvious fault of the subjective interpretation of the dFA test results which leads to poor sensitivity and a widely varying specificity, contrary to the claims made by the CDC:

"Direct fluorescent-antibody testing (DFA) provides a much more rapid result but also has the disadvantage of poor sensitivity, and its specificity varies widely due to the subjective interpretation of test results."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC85400/

This second study also points out the flaws of the subjective interpretation of the test results as well as the need for expensive equipment and quality-controlled reagents, the varied parameters utilized for succesful results and the issues relating to the incubation times and temperatures, as well as the necessity of having well-trained personnel running and interpreting the results:

"However, DFA has several drawbacks such as the need for an expensive fluorescent microscope, well-trained personnel, and quality controlled reagents (antibodies, conjugates), and varied parameters used during microscopy, and incubation times and temperatures, not to mention the subjectivity in interpretation of the test results [27,28,29,30]. In addition, acetone used as fixative in DFA does not completely inactivate the virus, as demonstrated by the infectivity of acetone-fixed tissue for neuroblastoma cells [31], posing a potential biohazard to laboratory personnel. Indeed, complete inactivation of cell culture-derived rabies virus appears to require >30% acetone [32]."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5876580/

And finally, from this 2017 study published in PLOS Neglected Tropical Diseases, we can once again see the problems with subjective interpretation of dFA test results in action. The study utilized 23 independent laboratories to aid in identifying "differences in the laboratory protocols that could explain discrepant laboratory results and provide baseline knowledge for regional standardization of protocols." The labs were each sent 20 samples which included 17 test samples and 3 controls. The positive tissues contained major rabies "virus" variants that were circulating in the Americas while the negative samples consisted of tissues demonstrating complete absence of rabies "virus" antigen and artifacts. Each lab was asked to test the samples using their own standard protocols and to record their results (positivity, intensity, and distribution of the fluorescence staining) as well as the microscopic condition and impression quality of the tissues (Good, Acceptable, or Deficient) as evaluated by the laboratory operator. The results from this 2017 study indicated that there are substantial differences in the overall dFA results and test interpretation as the "level of concordance between the 23 participating laboratories and the CDC panel showed large variability." Only two laboratories had 100% concordance, while 91% of the labs had at least one discordant sample, with a total of 26 false positive and 61 false negative results among all laboratories:

An inter- laboratory proficiency testing exercise for rabies diagnosis in Latin America and the Caribbean

"Our results indicate that although all laboratories can perform the direct fluorescent antibody test, there are substantial differences in the overall results and test interpretation. This study identified important gaps in standardization and/or harmonization between laboratories which could be overcome and corrected with appropriate DFA protocols standardized across the LAC, including its broad distribution and proper training."

"Conclusive rabies diagnosis can only be achieved by appropriate laboratory testing. Clinical and epidemiological diagnosis is challenging and leads to under-reporting [1, 2, 3]. The Direct Fluorescent Antibody test (DFA) for detection of rabies virus antigen remains as the gold standard test for laboratory diagnosis of rabies in post-mortem brain tissues [3]."

"The agreement between the laboratory results and those of the CDC, as measured by the sensitivity, specificity, concordance and kappa values are shown in Table 2. Two laboratories correctly identified all samples tested (sensitivity and specificity of 1.0). However, 30% (7/23) of all laboratories reported at least one false positive and 83% (19/23) of all laboratories reported at least one false negative sample. The average sensitivity was 76% with a range of 40% to 100%. The average specificity was 88% with a range of 22% to 100%. While a majority of the laboratories had low false positive rates, there were considerable differences in the sensitivity (Fig 1). The mean concordance was 81% with a range of 50% to 100% and the mean kappa score was 0.56 with a range of 0.02 to 1.00."

"The level of concordance between the 23 participating laboratories and the CDC panel showed large variability. Two laboratories had 100% concordance, while 91% of the labs had at least one discordant sample, with a total of 26 false positive and 61 false negative results among all laboratories."

"The type of conjugate may also affect the sensitivity of the DFA test (monoclonal cocktail versus polyclonal, in-house made versus commercial). For the current exercise, laboratories used commercial (65%) or in-house (35%) conjugates. A study of 12 rabies reference laboratories in Europe demonstrated that the variability of conjugates could potentially lead to discordant results and influence assay sensitivity [19]."

https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0005427

A bunch of glowing green dots means…absolutely nothing.

In answer to the claim by the CDC that "during the 50 years the direct fluorescent antibody (DFA) test has been used in the United States, there has been no indication it has failed to provide accurate clinical information on the rabies status of an animal for the purposes of treating an exposed person," we can safely conclude that this is obviously a false statement. The dFA test has been shown to have low sensitivity and a widely varying specificity as well as major issues relating to the subjective interpretation of the results based upon the person doing the interpreting. The 23 labs participating in the 2017 study had large variability in concordance with the CDC's own panel. Anyone looking at this indirect test with a shred of intellectual honesty can easily see that the CDC's "golden standard" rabies test does not look so golden anymore.

While the dFA test is the "go to" diagnostic measure in modern times, there are other methods available which can be used in an attempt to claim an animal is infected with the rabies "virus." One of these is the "isolation" of the "virus" in tissue and cell cultures, which used to be the "gold standard" method for proving a "virus" exists and is infectious. Oddly enough, the CDC stated that the supposed "isolation" of the rabies "virus" is not as sensitive nor as specific as the dFA test. How could this possibly be the case?

For one thing, it is admitted that the rabies "virus" does not actually produce the desired cytopathogenic effect (CPE) when cultured:

Detection of rabies virus replication: inoculation tests

"The other group of available techniques aim at detecting the replication of the virus on living substrates, e.g. cells. Virus isolation may be necessary to confirm inconclusive results in FAT/dRIT and for characterization of the virus strain. In neuroblastoma cells, rabies virus grows generally without cytopathic effect; once again it is necessary to use FAT to confirm the presence of rabies virus. After intracranial application, rabies induces clinical signs in mice that are relatively typical but have to be confirmed by FAT. Since cell culture is as sensitive as the mouse inoculation test, units should be established in laboratories to replace mouse inoculation tests as it avoids the use of life animals, is less expensive and gives more rapid results."

https://www.who-rabies-bulletin.org/site-page/diagnosis-rabies

Why is this important to note? The cytopathogenic effect (CPE) is the structural and morphological changes to the cell that are claimed to be caused by the "virus" as it enters the cell, breaking it apart as the "virus" creates more copies of itself. This effect is supposed to tell the researchers that the "virus" is present within the culture. According to their stories, without this effect, it should be a clear indicator that the host was not infected by the "virus." However, virology loves to bend their own rules and in a clear cut case of having their cake and eating it too, virologists claim that certain "viruses" do not cause CPE in their natural host cells. They state that there are different levels of CPE based on the cell type used:

  • Not permissive cell – virus cannot infect
  • Permissive cell – virus can replicate, but does not cause obvious CPE
  • Highly permissive cell – virus replicates and induces an obvious CPE

https://cytosmart.com/resources/virus-induced-cytopathic-effect

Anyone looking at this logically can see that "Not permissive" and "Permissive" cells are the exact same thing. Neither of these cells produce CPE when "infected" by the "virus." However, virologists will resort to other indirect measures in order to claim the "virus" is present in spite of the lack of any CPE observed. In the case of rabies, the dFA test is used to confirm if a "virus" is present in a culture. However, if the dFA test is considered inconclusive, the cell culture is used to confirm the dFA result. A bit circular there, don't you think? Another confirmation is done by injecting the toxic CPE-less cell culture soup into the brain of a mouse and seeing if symptoms occur. If so, the mouse is killed and the newly damaged brain is taken and tested by dFA for confirmation. Seeing the problem yet?

Toxic cell-cultured goo injected directly into the brain causing brain damage. It must be the "virus" and not the method… 🤷‍♂️

If neither dFA and/or cell culturing is enough satisfactory indirect evidence to claim the existence of the rabies "virus," one can turn to the old ways of histopathology to try and build a circumstantial case against the invisible entity. Along with attempting to diagnose someone based on clinical symptoms, which thanks to Louis Pasteur and "false rabies" we know is inaccurate due to the non-specificity of the symptoms, histopathology was the main method utilized for decades for determining if an animal was in fact rabid. This consisted of staining the brain tissues with chemicals such as hematoxylin and eosin and looking for patterns of encephalopathy as well as the presence of what are called Negri bodies. Negri bodies are round or oval inclusions within the cytoplasm of nerve cells of animals which were discovered by Dr. Adelchi Negri in 1903. At the time, he claimed that these inclusions were the etiologic agent of rabies. While the rest of the virology community disagreed with Dr. Negri, his discovery was considered a tell-tale sign of rabies infection in the brain and finding these inclusions served as the basis for a rabies diagnosis for over 60 years. However, there is rather big problem for these histopathological examinations. Signs of encephalitis and finding Negri bodies are both entirely non-specific and are seen in cases that have absolutely nothing to do with rabies. In fact, Negri bodies are said to only be found in half of the cases of rabies:

Histologic examination, General histopathology

"Histologic examination of biopsy or autopsy tissues is occasionally useful in diagnosing unsuspected cases of rabies that have not been tested by routine methods. When brain tissue from rabies virus-infected animals are stained with a histologic stain, such as hematoxylin and eosin, evidence of encephalomyelitis may be recognized by a trained microscopist. This method is nonspecific and not considered diagnostic for rabies.

Before current diagnostic methods were available, rabies diagnosis was made using this method and the clinical case history. In fact, most of the significant histopathologic features (changes in tissue caused by disease) of rabies infection were described in the last quarter of the 19th century. After Louis Pasteur's successful experiments with rabies vaccination, scientists were motivated to identify the pathologic lesions of rabies virus.

Histopathologic evidence of rabies encephalomyelitis (inflammation) in brain tissue and meninges includes the following:

  1. Mononuclear infiltration
  2. Perivascular cuffing of lymphocytes or polymorphonuclear cells
  3. Lymphocytic foci
  4. Babes nodules consisting of glial cells
  5. Negri bodies
Negri bodies

In 1903, most of the histopathologic signs of rabies were recognized, but rabies inclusions had not yet been detected. At this time, Dr. Adelchi Negri reported the identification of what he believed to be the etiologic agent of rabies, the Negri body. In his report, he described Negri bodies as round or oval inclusions within the cytoplasm of nerve cells of animals infected with rabies. Negri bodies may vary in size from 0.25 to 27 µm. They are found most frequently in the pyramidal cells of Ammon's horn, and the Purkinje cells of the cerebellum.

They are also found in the cells of the medulla and various other ganglia. Negri bodies can also be found in the neurons of the salivary glands, tongue, or other organs. Staining with Mann's, giemsa, or Sellers stains can permit differentiation of rabies inclusions from other intracellular inclusions. With these stains, Negri bodies appear magenta in color and have small (0.2 µm to 0.5 µm), dark-blue interior basophilic granules.

The presence of Negri bodies is variable. Histologic staining for Negri bodies is neither as sensitive nor as specific as other tests. Some experimentally-infected cases of rabies display Negri bodies in brain tissue; others do not. Histologic examination of tissues from clinically rabid animals show Negri bodies in about 50% of the samples; in contrast, the dFA test shows rabies antigen in nearly 100% of the samples. In other cases, non-rabid tissues have shown inclusions indistinquishable from Negri bodies. Because of these problems, the presence of Negri bodies should not be considered diagnostic for rabies."

https://www.geosalud.com/pets/rabies_diagnosis.html

Whoever wants to point at random circles seen in fixed and stained dead tissues and then make wild guesses about their importance, raise your hand! ✋

As the Negri bodies played such a substantial role in determining the diagnosis of rabies and building the case statistics used to sell the public on a "virus" in need of vaccination and eradication, let's look at two more studies to find out a bit more about these non-specific diagnostic blobs. In 1942, it was already well known that the Negri bodies were not specific to rabies and could be mistaken for other inclusion bodies seen in the tissues upon examination. This is a rather big deal as the mass vaccination of dogs didn't start for another 5 years in 1947. So we can already see that the main method used for diagnosis was faulty which casts doubt on any rabies statistics generated up to that time using this method. The authors go on to admit that there were deficiencies in the method used for examining these inclusions. It is stated that every experienced microscopist encountered difficulty in deciding whether or not the bodies observed were in fact Negri bodies or whether they were instead normal or possibly distorted cytoplasmic structures. In the study of 84 mice said to be given rabies by way of injection, Negri bodies were only found in the hippocampus 8 times as well as only 4 times in the cerebral cortex. The authors concluded that there are many rabies cases without Negri bodies present upon examination and that there are various structures which resemble Negri bodies commonly found in normal animals:

Problems in the Laboratory
Diagnosis of Rabies*

"THE diagnosis of rabies in the laboratory is based entirely upon the microscopic demonstration of Negri bodies and upon animal inoculation. The demonstration of Negri bodies is the method of choice since the diagnosis can be thus made in a few minutes or hours. When the technic employed demonstrates typical bodies the result is highly convincing and satisfying. However, negative and doubtful results leave much to be desired, and animal inoculation must be resorted to. The difficulties in demonstrating Negri bodies arise from two sources of error which can be enumerated as inability to differentiate them from other inclusion bodies and cell structures, and inherent deficiencies in the methods of examination."

"However, every experienced
microscopist has encountered the difficulty of deciding whether the bodies observed in some preparations are Negri bodies or cytoplasmic structures normal to the cell or if not normal at least only distorted cellular structures. Goodpasture refers to the variation in size of Negri bodies and speaks of being able to demonstrate the smallest forms. When small bodies are associated with large ones, which show the typical inner structure, no confusion is encountered. When, however, only forms so small occur that the demonstration of the "Innenkorper" is doubtful, the diagnosis is doubtful. The brain of cats, particularly, offers difficulty because of the pink staining granular material in the cells and also because the Negri bodies in the pyramidal and Purkinji cells of this animal are often very small. The failure of the microscopic diagnosis of rabies as proved by mouse inoculation is shown in Table 1."

"Above we have mentioned the occasional occurrence of what appear to be "lyssa bodies" or small Negri bodies in the brain of some animals which did not produce rabies when injected into mice. These bodies are found most frequently in the cerebrum and medulla. Since in the study of 84 cases of rabies proved by mouse inoculation we found Negri bodies only in the hippocampus 8 times and only in the cerebral cortex 4 times (Table 2), the finding of eosinophilic bodies in any portion of a brain from an animal suspected of having had rabies creates a doubt as to the diagnosis."

"From these results it appears that by microscopic examination of sections and in some smears we are able to demonstrate eosinophilic bodies resembling "lyssa bodies" and atypical Negri bodies which are not associated in the brain with rabies virus. Also the results show that brain specimens in which the microscopic examination leaves the diagnosis in doubt contain rabies. The bodies that cause this confusion in the microscopic diagnosis of rabies are similar to ones found in certain parts of the brain of normal cattle and other animals and to atypical or small Negri bodies."

doi: 10.2105/ajph.32.2.171.

While the 1942 study should have been the end of the Negri body as a diagnostic indicator of rabies, this method carried on being used over the decades. In 1975, another study emerged casting doubts on the dogma surrounding these long-held markers of the rabies disease. It's stated that there was a universal acceptance of the Negri body as a specific indicator of rabies and that due to this widely-endorsed dogma, every time a Negri body was seen, a rabies diagnosis was made irrespective of the circumstances regarding the case.

However, in this study, a case was reported of a person who was considered rabies free by way of dFA and electron microscopy but Negri bodies were still found upon examination. This finding was inconsistent with the idea of the specificity of these bodies to rabies. The author pointed out many flaws with the use of Negri bodies as a diagnostic tool as outside of finding them upon examination, rabies is non-specific and mimics other diseases such as smallpox. It is stated that rabies encephalitis does not have any pathognomonic clinical or pathologic features distinguishing it from other diseases. The absence of Negri bodies in a substantial number of fatal cases of rabies, the lack of any inflammatory response, the absence of any history of animal contact in more than 30% of fatal cases, and the lack of specific behavioral symptoms of rabies in animals led the author to the conclusion that any association between this diagnostic method and the rabies disease is unwarranted. Thus, it is easy to see that any and all rabies case statistics based upon the clinical diagnosis and findings of Negri bodies should be thrown out:

Is the Negri Body
Specific for Rabies?

"Of all viral diseases affecting
the nervous systems of humans and animals, rabies seems to be the only one in which light microscopy alone can provide a definitive etiologic diagnosis. This is based on the universally accepted conviction on the specificity of the Negri body for rabies. Thus, the presence of a Negri body in the brain of a patient who did not have rabies is a matter that deserves attention."

"Neuropathologically, the exclusion of rabies in the present case is based on the negative immunofluorescent
study results for rabies and the absence of the rabies virus within the Negri bodies (light microscope) as demonstrated by electron microscopy. Such an observation, of course, is inconsistent with the specificity of the Negri body in signifying the presence of rabies. Therefore, it is reasonable to ask: What are the other inclusion bodies that occur in sites other than the nervous system that are morphologically similar to Negri body?"

"The result of a universally accepted dogma such as this is obvious; in every instance in which a "Negri body" has been seen, a diagnosis of rabies was made irrespective of the circumstances.

To delineate some of the related aspects of the problem the following points deserve etnphasis:

  1. Except for the occurrence of the Negri body, rabies encephalitis does not have any pathognomonic clinical or pathologic features. Variola-vaccinia virus, for example, can produce the same clinical pictures. The cutaneous manifestations can be sufficiently scanty to be missed on the physical examination, or they can be absent altogether (variole sans eruptione). There is remarkable variability in the intensity of cellular inflammatory response in rabies encephalitis. This, to some extent, may reflect the vigor with which these reactions are searched for, since the diagnostic efforts in the past have been mainly directed to the "specific" finding of the Negri body. The absence of Negri bodies in a substantial number of fatal cases of rabies and the remarkable lack of inflammatory response in some instances of the disease signify the importance of obtaining a careful history. A definitive etiologic diagnosis of rabies, however, requires obtaining positive results with immunofluorescent or electron microscopical methods or both. The former method maps the occurrence of rabies viral antigen in any morphologic form (with or without the presence of the inclusions), and the latter defines the characteristic bullet-shaped virus.
  2. Absence of history of animal contact has been reported in more than 30% of fatal cases of rabies. Here, also, it is the unquestioned association between the Negri body and rabies that constitutes the sole ground for a definitive etiologic diagnosis. The latter report is remarkable for the absence of history of animal contact and the occurrence of the fatal illness one week after vaccination for smallpox. Even in the presence of history of animal contact, it should be remembered that such an association is unwarranted as the behavioral alterations in the animals are not pathognomonic of any one disease.
  3. It is conceivable that the failures of antirabies therapy and the occurrence of false negative immunofluorescent results are related to the non-specificity of the Negri body for rabies.
  4. In no other viral disease is the light microscopy alone an accepted method for the definitive etiologic diagnosis of a disease.

The validity of the present observations needs confirmation by other observers and the answer will be found "not by dogma or skepticism but by open-minded uncertainty."

doi: 10.1001/archneur.1975.00490440025002.

No single diagnostic test is sufficient.
In Summary:
  • According to the Institut Pasteur, Louis Pasteur's initial efforts to isolate the rabies "virus" proved unsuccessful as the "virus" remained invisible
  • The "virus" was not seen until almost a century later, in 1962, with the advent of electron microscopy
  • Louis Pasteur had the idea of inoculating part of a rabid dog's brain directly into another dog's brain, causing the inoculated dog to subsequently die
  • Inoculation with saliva (where the "virus" is supposedly found) was found to be a method which did not always produce rabies and symptoms did not declare themselves for months
  • Pasteur accordingly inoculated a number of animals subcutaneously with some of the brain substance from other animals which had died of rabies
  • Most of those inoculated developed rabies, but not all
  • Pasteur's idea of introducing into the brain of experimental animals some of the nerve tissue from an animal which had died of rabies was based on the principle (i.e. assumption)of providing the causal organisms with the nutritive medium best suited to their requirements
  • There is a very high degree of uncertainty in the correlation between animal bites and the subsequent appearance of rabies-even when the biting animal is certifiably rabid
  • While the mortality of clinical rabies is "virtually 100 percent," the threat of death from the bite of a rabid animal is vastly less
  • Estimates of the risk of contracting rabies from the bites of animals known to be rabid range from as high as 80 percent to as low as 0.5 percent
  • Pasteur himself estimated that 16 percent of those bitten by rabid dogs would eventually die of rabies unless they submitted to his new treatment
  • In 1887, the English Commission on Rabies drew attention to the uncertainty of all statistics on rabies citing:
    1. The difficulty of establishing that the attacking animal had in fact been rabid
    2. The variable effects of the location and depth of bites
    3. Differences in the lethality of rabid animal bites in different species and races
    4. The possible prophylactic effects of cauterization or other treatments applied to bitten victims before they submitted to Pasteur's treatment
  • The commission also suspected that at least one man may have died as a direct result of the Pastorian injections, and in the end it favored strict regulations on potentially rabid animals (muzzling and quarantine) over Pasteur's more drastic remedy
  • The great majority of the victims of rabid animal bites could forgo Pasteur's treatment without experiencing any untoward consequences in the future
  • Pasteur himself later pointed out some of the uncertainties surrounding the diagnosis of rabies
  • Pasteur cited two cases in which symptoms of the disease had been induced solely by fear without any animal bite as well as another case which was induced by alcoholism
  • Pasteur had a vested interest in emphasizing the difficulty of diagnosing rabies as he was then defending himself against allegations that his rabies vaccine not only sometimes failed to protect those who submitted to it, but in some cases was itself the cause of rabies and therefore death
  • In defense of his vaccine, Pasteur now emphasized the extent to which symptoms like those of rabies could appear in patients who did not have the disease
  • According to the CDC, the diagnosis of rabies can be made after detection of rabies "virus" from any part of the affected brain, preferably the brain stem and cerebellum
  • The test requires that the animal be euthanized
  • According to biologist Harold Hillman: "Killing an animal changes its biochemistry grossly. For example, its blood carbon dioxide, phosphate, lactate, and potassium ion concentrations, rise, while its oxygen, sodium ion, adenosine triphosphate, phosphocreatine, concentrations go down. These changes affect much of the tissue metabolism."
  • Hillman felt that "it is worth asking whether cell biologists should use tissues in vitro at all"
  • The current "gold standard" test used to detect the "virus" on the brain tissue is the direct fluorescent antibody test (dFA)
  • The dFA test is based on the "observation" that animals infected by rabies "virus" have rabies "virus" proteins (antigen) present in their tissues
  • Because rabies is present in nervous tissue (and not blood like many other "viruses"), the ideal tissue to test for rabies antigen is brain
  • When labeled antibody is incubated with rabies-suspect brain tissue, the story goes that it will bind to rabies antigen and unbound antibody can be washed away so that areas where antigen is present can be visualized as fluorescent-apple-green areas using a fluorescence microscope
  • According to the CDC, during the 50 years the direct fluorescent antibody (DFA) test has been used in the United States, there has been no indication it has failed to provide accurate clinical information on the rabies status of an animal for the purposes of treating an exposed person
  • The CDC states that because of its high sensitivity and specificity, in comparison to "virus" isolation methods, the DFA test is the "gold standard" diagnostic method for rabies (way to shoot "virus" isolation in the foot there CDC…)
  • During clinical disease, millions of "viral" particles may be found intermittently in the saliva (which makes one wonder why they must kill an animal and do indirect antibody tests on decomposing brain tissue for diagnosis rather than properly purify and isolate the "virus" directly from the saliva supposedly containing millions of these entities)
  • In theory, only a single rabies particle or "virion" is required to result in a productive infection
  • The dFA results are based upon the opinion of an interpreter who uses an antigen fluorescence intensity and distribution scale from +4 on down to +1 to determine one of four conclusions: positive, negative, unsatisfactory, or inconclusive
  • The dFA test has the disadvantage of poor sensitivity, and its specificity varies widely due to the subjective interpretation of test results
  • DFA has several drawbacks such as:
    1. The need for an expensive fluorescent microscope
    2. Well-trained personnel
    3. Quality controlled reagents (antibodies, conjugates)
    4. Varied parameters used during microscopy
    5. Incubation times and temperatures
    6. The subjectivity in interpretation of the test results
  • According to a 2017 study testing and reviewing dFA with the help of numerous labs, the results indicated that although all laboratories can perform the direct fluorescent antibody test, there are substantial differences in the overall results and test interpretation
  • The authors stated that conclusive rabies diagnosis can only be achieved by appropriate laboratory testing as clinical and epidemiological diagnosis is challenging and leads to under-reporting
  • The agreement between the laboratory results and those of the CDC, as measured by the sensitivity, specificity, concordance and kappa values:
    1. Only two laboratories correctly identified all samples tested (sensitivity and specificity of 1.0)
    2. However, 30% (7/23) of all laboratories reported at least one false positive and 83% (19/23) of all laboratories reported at least one false negative sample
    3. The average sensitivity was 76% with a range of 40% to 100%
    4. The average specificity was 88% with a range of 22% to 100%.
    5. While a majority of the laboratories had low false positive rates, there were considerable differences in the sensitivity
    6. The mean concordance was 81% with a range of 50% to 100% and the mean kappa score was 0.56 with a range of 0.02 to 1.00
  • The level of concordance between the 23 participating laboratories and the CDC panel showed large variability
  • Two laboratories had 100% concordance, while 91% of the labs had at least one discordant sample, with a total of 26 false positive and 61 false negative results among all laboratories
  • The type of conjugate may also affect the sensitivity of the DFA test (monoclonal cocktail versus polyclonal, in-house made versus commercial)
  • A study of 12 rabies reference laboratories in Europe demonstrated that the variability of conjugates could potentially lead to discordant results and influence assay sensitivity
  • Another method for diagnosing rabies is the "isolation" of the "virus" by tissue or cell culture
  • "Virus isolation" may be necessary to confirm inconclusive results in dFA/dRIT and for characterization of the "virus" strain
  • In neuroblastoma cells, rabies "virus" grows generally without cytopathic effect
  • In a bit of cirular reasoning, it is necessary to use dFA to confirm the presence of rabies "virus" by way of cell culture whereas cell culture may also be used to confirm inconclusive dFA results
  • After intracranial (in the brain…some things never change) application, rabies induces clinical signs in mice that are relatively typical but have to be confirmed by dFA (i.e. the mouse that has had toxic cell culture goo injected into its brain causing symptoms must then be killed to have its cell-culture damaged brain examined by dFA to confirm the infection)
  • Histologic examination of biopsy or autopsy tissues looking for signs of encephalitis is occasionally useful in diagnosing unsuspected cases of rabies that have not been tested by routine methods
  • However, this method is nonspecific and not considered diagnostic for rabies
  • Before current diagnostic methods were available, rabies diagnosis was made using this method and the clinical case history (i.e. non-specific and not suited for diagnostic methods were used to identify rabies for most of the 19th and 20th century)
  • Histopathologic evidence of rabies encephalomyelitis (inflammation) in brain tissue and meninges includes the following:
    1. Mononuclear infiltration
    2. Perivascular cuffing of lymphocytes or polymorphonuclear cells
    3. Lymphocytic foci
    4. Babes nodules consisting of glial cells
    5. Negri bodies
  • In 1903, Dr. Adelchi Negri reported the identification of what he believed to be the etiologic agent of rabies, the Negri body
  • In his report, he described Negri bodies as round or oval inclusions within the cytoplasm of nerve cells of animals infected with rabies
  • While this was the main method of diagnosing rabies for over 60 years, the presence of Negri bodies is variable
  • Histologic staining for Negri bodies is neither as sensitive nor as specific as other tests
  • Some experimentally-infected cases of rabies display Negri bodies in brain tissue; others do not
  • Histologic examination of tissues from clinically rabid animals show Negri bodies in about 50% of the samples
  • In other cases, non-rabid tissues have shown inclusions indistinquishable from Negri bodies
  • Because of these problems, the presence of Negri bodies should not be considered diagnostic for rabies
  • Despite these problems, until the mid-1960's the diagnosis of rabies in the laboratory was based entirely upon the microscopic demonstration of Negri bodies and upon animal inoculation
  • According to a study from 1942, the demonstration of Negri bodies was the method of choice since the diagnosis can be thus made in a few minutes or hour
  • However, the authors admitted that the difficulties in demonstrating Negri bodies arose from two sources of error which could be enumerated as the inability to differentiate them from other inclusion bodies and cell structures, and inherent deficiencies in the methods of examination
  • Every experienced microscopist has encountered the difficulty of deciding whether the bodies observed in some preparations are Negri bodies or cytoplasmic structures normal to the cell or if not normal at least only distorted cellular structures
  • In the study of 84 cases of rabies proved by mouse inoculation they found Negri bodies only in the hippocampus 8 times and only in the cerebral cortex 4 times
  • The authors determined that the finding of eosinophilic bodies in any portion of a brain from an animal suspected of having had rabies creates a doubt as to the diagnosis
  • From their results it appeared that by microscopic examination of sections and in some smears, they were able to demonstrate eosinophilic bodies resembling "lyssa bodies" and atypical Negri bodies which are not associated in the brain with rabies "virus"
  • Also the results showed that brain specimens in which the microscopic examination leaves the diagnosis in doubt contain rabies (i.e. they determined that injecting mice in the brain caused rabies without finding Negri bodies)
  • The bodies that cause this confusion in the microscopic diagnosis of rabies are similar to ones found in certain parts of the brain of normal cattle and other animals and to atypical or small Negri bodies
  • In a 1975 study, it is stated that rabies is the only "virus" that can be diagnosed by light microscopy based on the universally accepted conviction on the specificity of the Negri body for rabies
  • However, the authors presented a case of a patient without rabies as determined by negative immunofluorescent study results for rabies and the absence of the rabies "virus "within the Negri bodies (light microscope) as demonstrated by electron microscopy
  • Such an observation was inconsistent with the specificity of the Negri body in signifying the presence of rabies
  • The result of this universally accepted dogma led to every instance in which a "Negri body" was seen being diagnosed as rabies irrespective of the circumstances
  • Except for the occurrence of the Negri body, rabies encephalitis does not have any pathognomonic clinical or pathologic features (i.e. non-specific and overlapping symptoms associated with many diseases)
  • Variola-vaccinia (Smallpox) "virus," for example, can produce the same clinical pictures
  • There is remarkable variability in the intensity of cellular inflammatory response in rabies encephalitis
  • The diagnostic efforts in the past have been mainly directed to the "specific" finding of the Negri body
  • The absence of Negri bodies in a substantial number of fatal cases of rabies and the remarkable lack of inflammatory response in some instances of the disease signify the importance of obtaining a careful history
  • Absence of history of animal contact has been reported in more than 30% of fatal cases of rabies
  • In these cases, it is the unquestioned association between the Negri body and rabies that constitutes the sole ground for a definitive etiologic diagnosis
  • Even in the presence of history of animal contact, it should be remembered that such an association is unwarranted as the behavioral alterations in the animals are not pathognomonic of any one disease (i.e. there are many diseases which are said to cause the same symptoms in animals)
  • It is conceivable that the failures of antirabies therapy and the occurrence of false negative immunofluorescent results are related to the non-specificity of the Negri body for rabies
  • In no other "viral" disease is the light microscopy alone an accepted method for the definitive etiologic diagnosis of a disease
  • The author concludes that the answers to the observations made will be found "not by dogma or skepticism but by open-minded uncertainty."

When one looks into the history of rabies and the methods used to diagnose the disease, it becomes undeniable that the mythical status that surrounds this fear-based fictional narrative fed to the masses throughout the centuries is entirely unjustified and unwarranted. There is literally nothing there in support of rabies as a distinct disease caused by a specific "virus" that is transmitted to humans through the bite of a sick animal. If we were to lay out the facts in front of a jury, it would be an easy conviction:

  1. The pivotal moments of discovery in the late 19th century were built upon the fraudulent foundations laid out by Louis Pasteur, a man who manipulated and massaged his own data in order to sell his theories and his vaccine for fame and fortune.
  2. The supposed "isolation" of the "virus" didn't even take place until nearly a century after Pasteur admitted to never identifying a causative agent and yet it missed the necessary requirement of showing any indirect evidence of the "virus" highjacking the cell as the culture lacked any evidence of the cytopathogenic effect.
  3. The actual correlation between animal bites and symptoms of disease was considered highly uncertain and those who were attacked and bitten by clearly rabid animals could easily forgo any treatments without any ill health effects.
  4. The incubation period for the disease is inconsistent and is said to range anywhere from 6 weeks on up to 25 years before the development of symptoms.
  5. The severe symptoms associated with rabies are a rare occurrence in nature and are in fact seen most frequently as an adverse reaction to the vaccine said to contain neurotropic ingredients.
  6. The acknowledgment by Pasteur of "false rabies," which was said to be brought about solely by FEAR of aquiring the disease as well as alcohol and/or drug use, was used to take attention away from his vaccine causing injury and death.
  7. The statistics regarding rabies cases were considered unreliable due to the lack of any specifuc disease-defining symptoms as many diseases in animals and humans mimic the clinical picture.
  8. The diagnosis of rabies, for much of its history, relied upon clinical symptoms and the histopathological findings related to encephalitis and Negri bodies, all of which are non-specific and are not suitable as a diagnostic measure for the disease, thus calling into question any case statistics related to rabies.
  9. The only way to claim pathogenicity of the "virus" is by way of the completely unnatural route of intracranial inoculation of diseased brain and nervous tissues directly into the brains of dogs and mice.
  10. The more recent modern method of direct fluorescence antibody tests, considered the "gold standard" diagnostic test, is claimed to be highly sensitive and specific, yet the results of the tests are open to human interpretation and have been shown in reviews to have low sensitivity and varied specificity.

The narrative surrounding rabies is based upon many primal fears. It plays on the fear of death, the fear of the unknown, and the fear of mutilation. Just like the rabid animal lurking in the shadows ready to strike, the "virus" hides inside the body once infected, waiting for the right moment to unleash a painful and excruciating death unless the infected leaps for the miracle cure in time. If they are a moment too late and the symptoms set in, it's game over. This same scenario is regularly sold to the masses in our daily entertainment with the recent zombie craze. One must be afraid of the bite. Once bitten, the "virus" takes hold and the victim is condemned to certain death.

WHO on Rabies:

"Human-to-human transmission through bites or saliva is theoretically possible but has never been confirmed."

https://www.who.int/news-room/fact-sheets/detail/rabies

However, just as Louis Pasteur recounted tales of the fearful succumbing to the exact same symptoms in absence of any animal bite, we must realize that the real enemy here is not a "virus" but an ingrained fear that stems from outdated and unproven fictional narratives. Moreso than any of the other more common diseases of the time such as smallpox and syphilis, rabies was the perfect mascot to convince the doubting public that disease-causing pathogens exist, can be transmitted, and can be prevented by way of vaccination. The imagery of the dirty mangled dog stumbling down the road, frothing at the mouth and seeking its next victim to transfer its parasitic contents into was a powerful visual tool for pathogens that remained nothing but formless thoughts at the time.

Dog with Rabies engraving from 1800.

However, the evidence consistently shows us that there is no dangerous invisible entity waiting in the wings inside the saliva of a rabid animal looking to seep into the open wound of a bite mark. There is no reason for any victim of an animal attack to subject themselves to the toxic treatments based upon the fear of an impending gruesome death. Just as there are no zombies coming for your brains, there is no frothing rabies "virus" looking to do the same. The foundation for germ theory and vaccination established by Pasteur was never built from any purified and isolated "virus" shown scientifically to exist in nature. It was built upon the only "virus" that has ever truly existed: the "virus" of fear.

For an excellent breakdown of the rabies fraud, please see Dr. Sam Bailey's What About Rabies? video:

What About Rabies?
ViroLIEgy
3 Aug 2022 | 2:56 pm

Blindsided by Rabies with Michael Wallach on the Skeptico Podcast


A few weeks ago, I was invited by Michael Wallach, the director of the amazing docu-series The Viral Delusion, to join him as a guest on the Skeptico podcast. It was an interesting experience to say the least. We were under the impression that the conversation would be focused on the gain of function/lab leak theories as well as HIV and we had prepared ourselves to discuss these topics. However, the conversation instead took a detour when the host, Alex Tsakiris, changed the focus to rabies instead, an area he felt was left unexplained by those of us stating that "viruses" do not exist. He presented us with a graph showing statistics of rabies cases declining with the use of vaccines. Unfortunately, at the time that we were interviewed, Alex was unable to provide us with a source for the information that he shared with us. Neither Michael nor I had ever seen this graph before, however it really wasn't the issue as vaccine statistics do not prove a "viral" cause.

Unfortunately, the rabies graph became the bulk of our time on the show. Michael Wallach did an excellent job explaining the problems with the lack of evidence behind the rabies "virus" as well as the fraud of Louis Pasteur. I wanted to chime in more to help out (not that Michael needed me to) but sadly Alex was not really interested in what I had to say about the subject. You can view our conversation with Alex on the Skeptico podcast here:

Michael Wallach, Rabies, Damn Rabies |561|

As I was unable to speak much on the topic with Alex, I want to present some information here that may help to answer his questions as to why rabies cases appeared to decline as the vaccine was introduced. However, before addressing the graph, the first thing that needs to be understood is that at no time has a rabies "virus" ever been properly purified and isolated directly from the fluids of any animal nor any human and then proven pathogenic by adherence to the scientific method. In fact, as he performed his experiments in the 1870's and 1880's, Louis Pasteur provided no theoretical basis for the vaccination of rabies as he admitted that he had failed to isolate the microbe that was presumed responsible for the disease. He also massaged and manipulated his data in order to justify his claims as to the success of rabies vaccination. Pasteur was a fraud who was more concerned with fame and prestige rather than performing valid scientific research. I wrote about his unethical practices involved with the early rabies research as well as how the rabies vaccines actually produced the severe neurological symptoms often associated with the disease here.

Later attempts to propagate the "virus" in the 1950's, which were claimed to be successful, were done in hamster brain and kidney cultures. Interestingly, it was noted that no cytopathogenic changes, the very criteria used by virologists to claim 'viruses" are present within these cultures, occured whatsoever.

doi: 10.3181/00379727-98-23997.

Even by the CPE standards used by virologists as a measure for the successful isolation of a "virus," they had failed to "isolate" rabies in their cultured samples. As no rabies "virus" has ever been scientifically proven to cause the disease, there is no basis to claim that the symptoms associated with rabies are caused by a "virus." Still, in spite of being given this information, Alex continued to focus on his graph as if the effect credited to the vaccine was somehow proof of a "viral" cause. However, one can not look to an effect in order to claim a cause. This is a logical fallacy known as affirming the consequent. It is often stated like this:

In other words, if rabies is caused by a "virus," the vaccine will lower cases. The cases declined with vaccine use, therefore rabies is caused by a "virus." Obviously, this is not a logical statement as there are many variables and factors unaccounted for that could lead to the appearance of a vaccine having a positive effect on rabies cases. It should also not need to be stated that just because a vaccine appeared to work does not mean that the cause of rabies was a "virus." A rabies "virus" must be scientifically proven to exist first in order to be tested for as the cause of the symptoms of disease associated with it. This has never been done.

We therefore must ask ourselves a very important question:

  • Did the rabies vaccines really cause rabies cases to fall or are there other potential reasons for the apparent decline?

Let's try to answer this by looking at the graph Alex provided on the air. Fortunately, I was able to find the source for the image. It came from the CDC's own data from the Morbidity and Mortality Weekly Report in July 2019. The study was titled Vital Signs: Trends in Human Rabies Deaths and Exposures — United States, 1938–2018.

As usual, cases in both humans and animals dropped well before the vaccine was introduced. https://www.cdc.gov/mmwr/volumes/68/wr/mm6823e1.htm

What we can find out is that rabies cases were exceedingly rare over the entire graph period, with only 588 cases of human rabies reported in the United States from 1938 to 2018. In fact, there was a sharp decline in rabies cases a few years prior to the mass vaccination of dogs in 1947, which is often the case when looking at the decline in disease before the introduction of vaccination. Of course, the vaccine is given the credit even though the cases were well in decline beforehand.

So what could have caused this sharp drop before and after vaccine introduction? If you have looked into the decrease in diseases claimed to have been caused by other "viruses," it is easy to spot a certain trend. Often times, the symptoms of disease claimed to be declining due to vaccination are reclassified either as a new or related disease caused by a new or related "virus." Smallpox was rebranded as chicken and/or monkeypox, polio became acute flaccid myelitis, syphilis morphed into AIDS, influenza transformed into "Covid," etc. etc. etc. This trend of rebranding and relabelling the same symptoms of disease as either new diseases or similar ones can easily be seen with rabies and the rabies-related "lyssaviruses." While the rabies "virus" is considered a "lyssavirus," there are numerous other "viruses" under this same heading that are considered "rabies-like viruses" that do not cause rabies per se but instead "rabies-like" disease:

Rabies and Rabies-Related Lyssaviruses

"Closely related lyssaviruses circulate among bats in the Eastern Hemisphere, and can cause an illness identical to rabies. Rabies vaccines and post-exposure prophylaxis can provide some protection against some of these viruses, but not others. Rabies-related lyssaviruses can be found even in countries classified as rabies-free."

"Information about rabies-related lyssaviruses is currently limited to a small number of case reports and a few reports of experimental inoculation; however, the illness 
appears indistinguishable from rabies. Bats may either have mild or no clinical signs and survive the infection, or develop severe neurological signs and die."

https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.cfsph.iastate.edu/Factsheets/pdfs/rabies.pdf&ved=2ahUKEwiZg_vTlKb5AhVQIDQIHQUUBn8QFnoECA4QBg&usg=AOvVaw1sUN6nrW39qtkymm3HGt_r

According to the CDC, these rabies-related "viruses" include:

  1. Lagos bat
  2. Mokola "virus"
  3. Duvenhage "virus"
  4. European bat "virus" 1 & 2
  5. Australian bat "virus"

This is a nice convenient scapegoat which allows a country to declare itself rabies-free even though the same symptoms of disease still persist. For example, in Austraila you will find disclaimers such as this:

https://www.health.gov.au/diseases/rabies

According to Austrailia, they are rabies-free even though the same symptoms of disease persist within the country. These cases are blamed on the Australian bat "virus" which is claimed to cause a "rabies-like" disease. Quite convenient, right? However, what if the classification system for these "lyssaviruses" were to change? Would a country that is considered rabies-free lose its illustrious status?

Lyssaviruses and rabies: current conundrums, concerns, contradictions and controversies

"With increasing ICTV debate toward unification of virus taxonomy based on genetic distances, in the near future there may be a re-classification attempt, in which all phylogroup I viruses are segregated into one species (for example, Rabies lyssavirus?) and all phylogroup II viruses are segregated into another. Of course, such re-classification would miss important characteristics used for species demarcation at present and may have potential socio-economic or bio-political consequences for certain areas. For example, some places where RABV is not thought to circulate, such as in Australia or Western Europe (but where other lyssaviruses are present among bats), might lose their self-defined "rabies-free" status, on the basis of viral taxonomic re-organization, creating greater confusion, with potential public health, veterinary, or economic repercussions, if suddenly recast into the same disease status as Africa, Asia and the New World. Arguably, the term "rabies" appears to garner greater weight and seriousness than the less familiar designation "bat lyssavirus".

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5325067/

The loose definitions allow countries such as Austrailia to claim rabies-free status even though the disease still persists there. If the definition and/or classification changes, so to will their status. This is similar to how America is allowed to claim it has been polio-free since 1979 while there are cases every year of acute flaccid myelitis and other polio-like diseases which present with the same sets of symptoms. We could easily relabel those polio-like diseases as polio and lose the polio-free designation.

While the same set of rabies symptoms can be blamed on the closely related "lyssaviruses," they can also be blamed on unrelated "viruses" and conditions that are said to be caused by different "viruses," bacteria, genetic abnormalities, and even poisons.. For instance, animals can be diagnosed with distemper instead of rabies. These two diseases have often been confused for one another as the symptoms are indistinguishable:

Raccoons – distemper and rabies

"Canine distemper in raccoons starts slowly, with respiratory infections then they develop pneumonia. In the final stage of the disease, the raccoon may begin to wander aimlessly in a circle with bizarre behaviour as a result of brain damage. Many of these symptoms are similar to rabies – which can only be determined by laboratory testing."

https://www.delta-optimist.com/archive/blog-raccoons-distemper-and-rabies-3068619

What is canine distemper virus in dogs?

"CDV is a highly contagious paramyxovirus that affects dogs and wildlife including raccoons, skunks, grey foxes, and ferrets. This virus is closely related to the human measles virus, and can lead to respiratory, gastrointestinal (GI), and central nervous system (CNS) problems. CDV is often confused with other infectious diseases, including rabies, because the organ systems affected and clinical signs are similar."

Canine Distemper: Ensure Your Dog is Protected

There are many other diseases such as encephalitis and different neurological disorders which are also said to mimic rabies in animals. Even poisoning is stated to mimic the severe stages of the disease:

Diseases that can look like Rabies

"Encephalitis is one condition that can look somewhat like the early stages of rabies. In this condition, with is immune based in most dog breeds of dogs, the dog's own immune system begins to attack the brain. The result is a dog that may be confused, appear to stagger and bump into things, or even a dog that seems very disoriented and lost even in familiar settings. The dog may also have temperament changes and may snap at owners or become very agitated when they have previously been calm and friendly."

"Canine distemper is another disease that may be mistaken for rabies since the symptoms are so close to being the same. Even wild animals such as raccoons, foxes and coyotes can have distemper that can even further confuse the issue. Since it is still a highly contagious disease it is essential to get your dog to the vet if he or she has had any contact with wild animals or other dogs that seem to be disoriented, have a discharge from the eyes or nose, paralysis and stumbling types of movements. Typically the wild animal will be non-threatened by human presence, which in itself is a sign of abnormal behavior. It is important to realize that distemper, unlike rabies, cannot be passed from an animal to a human. However it is important to stay away from any animal that appears to have any symptoms similar to rabies or distemper."

"Other neurological conditions, some which are fatal and contagious and some that are strictly a result of a genetic or inherited condition can mimic the early signs of rabies. In rare cases animals that are poisoned and those with neurological conditions can exhibit the same signs as advanced stages of rabies including paralysis, drooling, sensitively to light and sound, dramatic changes in behavior and even refusal to eat or drink."

https://terrificpets.com/articles/102287565.asp

As can be seen from the above three sources, canine distemper and other diseases such as encephalitis can be confused with rabies due to the identical nature of the symptoms. These diseases still persist within dogs and other animals while rabies, or at least "dog rabies," has been said to have been eliminated from the US and other countries. In other words, the rabies label is no longer applied upon diagnosis even though the same symptoms of disease circulate in animals within the country.

This merry-go-round among the same symptoms of disease does not stop with animals either. There are many conditions in humans that also mimic rabies. These diseases are outlined in this final source:

Beware: there are other diseases that can mimic rabies:
  • Diseases that can mimic encephalitic rabies:
    1. viral encephalitis (i.e. Japanese, eastern equine, West Nile)
    2. delirium tremens
    3. acute substance intoxication (i.e. cocaine, amphetamines)
    4. acute psychoses
    5. bacterial meningitis
    6. cerebral malaria
    7. post-rabies vaccination encephalopathy
    8. bite of an elapid snake (i.e., cobra)
    9. tetanus
  • Diseases that can mimic paralytic rabies:
    1. polio
    2. Guillain–Barré syndrome
    3. botulism
    4. diphtheria
    5. bite of an elapid snake (i.e., cobra)

Rabies
Rabies? Or Zombie bite…?
In Summary:
  • Louis Pasteur admitted to not isolating the agent presumed to cause rabies
  • In the 1950's, attempts to isolate the "virus" in cultures of hamster brains and kidneys were deemed successful despite the lack of observing any cytopathogenic effect (CPE)
  • Many "viruses" that are said to be eliminated or controlled through vaccination were rebranded and relabelled as either similar diseases caused by related "viruses" or new diseases caused by new "viruses"
  • Regarding rabies, closely related "lyssaviruses" circulate among bats in the Eastern Hemisphere and can cause an illness identical to rabies
  • Rabies-related "lyssaviruses" can be found even in countries classified as rabies-free
  • The illness associated with these rabies-related "lyssaviruses" appears indistinguishable from rabies
  • Some places where rabies is not thought to circulate, such as in Australia or Western Europe (but where other "lyssaviruses" are present among bats), might lose their self-defined "rabies-free" status, on the basis of "viral" taxonomic re-organization,
  • This would create greater confusion, with potential public health, veterinary, or economic repercussions, if they were suddenly recast into the same disease status as Africa, Asia and the New World
  • The term "rabies" appears to garner greater weight and seriousness than the less familiar designation "bat lyssavirus"
  • Canine distemper is a rabies-like illness in animals
  • In raccoons, it starts slowly, with respiratory infections then they develop pneumonia
  • In the final stage of the disease, the raccoon may begin to wander aimlessly in a circle with bizarre behaviour as a result of brain damage
  • Many of these symptoms are similar to rabies – which can only be determined by laboratory testing
  • Canine distemper is often confused with other infectious diseases, including rabies, because the organ systems affected and clinical signs are similar
  • It is mistaken for rabies since the symptoms are so close to being the same
  • Even wild animals such as raccoons, foxes and coyotes can have distemper that can even further confuse the issue
  • Encephalitis is another condition that can look somewhat like the early stages of rabies
  • The result of this brain swelling is a dog that may be confused, appear to stagger and bump into things, or even seems very disoriented and lost even in familiar settings
  • Other neurological conditions, some which are fatal and contagious and some that are strictly a result of a genetic or inherited condition can mimic the early signs of rabies
  • In rare cases animals that are poisoned and those with neurological conditions can exhibit the same signs as advanced stages of rabies including paralysis, drooling, sensitively to light and sound, dramatic changes in behavior and even refusal to eat or drink
  • In humans, there are many diseases which mimic rabies:
    1. Diseases that can mimic encephalitic rabies:
      • "viral" encephalitis (i.e. Japanese, eastern equine, West Nile)
      • delirium tremens
      • acute substance intoxication (i.e. cocaine, amphetamines)
      • acute psychoses
      • bacterial meningitis
      • cerebral malaria
      • post-rabies vaccination encephalopathy
      • bite of an elapid snake (i.e., cobra)
      • tetanus
    2. Diseases that can mimic paralytic rabies:
      • polio
      • Guillain–Barré syndrome
      • botulism
      • diphtheria
      • bite of an elapid snake (i.e., cobra)

For some reason, people seem to think rabies is a "gotcha" for those of us claiming that "viruses" do not exist. This disease is thrown out as proof that vaccines are effective and that because of this, the "virus" must therefore exist. However, a big problem for anyone championing rabies as proof for the existence of "viruses" continues to be the lack of any purified and isolated "virus" particles coming directly from the fluids of a rabid host. Louis Pasteur openly admitted to failing to meet this burden of proof even though he subjected animals and humans to experimental injections. Attempts by researchers in the 1950's to propagate the "virus" in tissue and cell cultures did not produce the characteristic cytopathogenic effect said to be necessary in order to determine if a "virus" is present in a culture. Thus, there is no scientific proof for the existence of the rabies "virus," even by virology's own standards.

As the rabies "virus" can not be shown to exist, any data relating to a decrease in cases due to a vaccine which is then used as proof for the existence of a rabies "virus" is entirely irrelevant. There are many reasons to doubt case statistics as these can be easily manipulated and massaged in order to create whatever narrative is desired. It can be seen that the same symptoms associated with rabies still exist today as there are many other diseases either said to be caused by rabies-related "viruses" or completely unrelated "viruses" that share the exact same symptoms associated with rabies. These diseases are more commonly diagnosed in areas where rabies is said not to be circulating. It is very apparent that virology loves to rebrand and relabel the same symptoms of disease as multiple "new and different" diseases in order to create the perception that the treatments work. This is why places like Austrailia get to claim to be "rabies-free" even though a rabies-like disease said to be caused by a rabies-like "virus" still exists there. This lowers the cases as the older diseases are claimed to be either eradicated and/or under control due to "successful" vaccination campaigns and thus they are not looked for as a diagnosis. There is no way that these statistics can be trusted when the definitions and labels of what is or is not rabies seemingly changes at will.

In any case, the rabies statistics are a moot point. Until someone can provide proof of the purification and isolation of the particles assumed to be rabies directly from the fluids of a rabid host which were proven pathogenic in a natural way, these case numbers are utterly meaningless. The conversation with Alex on the Skeptico podcast should have never even reached vaccination statistics unless he provided a paper showing the evidence for the existence of a rabies "virus" first. Unfortunately, while Michael did an admirable job defending our position, we were not prepared for the graph and did not get the chance to look over the data and present our counter-argument. Hopefully we can get the chance to go on again and discuss the issue in further detail in the future. However, if not, this response will have to suffice.

ViroLIEgy
28 Jul 2022 | 1:30 pm

A Follow Up to the “Virus” Challenge: 7/27/22 Dr. Tom Cowan Webinar With Dr. Andrew Kaufman, Mike Stone, and Mike Donio


Yesterday, I had the absolute pleasure and honor of being on Dr. Tom Cowan's Wednesday webinar to discuss a follow-up on the No "Virus" Challenge. We addressed a paper that was supplied by Steve Kirsch and Co. as the "irrefutable evidence" for the existence of "SARS-COV-2." The paper, a June 2022 non peer-reviewed preprint written by Dr. Sin Lee, is nothing but meaningless genomic data based on a fraudulent "SARS-COV-2" genome from January 2020. For some reason, the Fan Wu paper supplying the original fraudulent genome was not presented as "irrefutable evidence." Also discussed are cyro-EM images said to be considered evidence of live "virus." Please watch the webinar and find out why neither the genomic data nor the EM images constitute "irrefutable evidence" of a "virus" that was never purified and isolated.

Live Webinar With Dr. Andrew Kaufman, Mike Stone, and Mike Donio – Recorded on July 27th, 2022

In this webinar, along with Dr. Andrew Kaufman, Mike Stone & Mike Donio, we discussed the Virus Challenge in further detail.
We also reviewed the following article by Sin Hang Lee, which can be found here: https://www.preprints.org/manuscript/202206.0192/v1

Follow along for more Virus Challenge updates at: https://drtomcowan.com/pages/the-virus-challenge

Watch here: https://www.bitchute.com/video/rekrHZ52IKZy/

ViroLIEgy
26 Jul 2022 | 3:56 am

The “Virus” of Sin


What constitutes proof for the existence of an entity such as a "virus?" It is safe to say that most would agree that having the particles assumed to be the "virus" taken directly from the fluids of a sick host and having them physically present in a pure and isolated state so that the particles can be examined and manipulated would be a good place to start. It would then be possible to photograph the particles in order to determine the morphology and structure of the assumed "virus" and to determine the purification of the sample by showing whether or not there are other microorganisms present that could also potentially be correlated to disease. Researchers would then be able to take the purified and isolated particles and biochemically characterize and sequence them. It would then be possible to use these purified and isolated particles in an attempt to prove pathogenicity by subjecting a healthy host to the particles via a natural route in order to see if they can cause the same symptoms of disease that they are suspected of causing. This entire process would be repeated again and again in order to see if the same purified and isolated particles are found in each host and to see if they can cause the exact same symptoms each and every time. This would be the logical approach and one that adheres to the scientific method.

What does not constitute proof for the existence of an entity such as a "virus?" Most would agree that ignoring all of the steps outlined above, buying a commercially-made lab-created cell culture concoction said to contain the "virus," taking this unpurified mixture and sequencing it, and then claiming that the resulting computer-generated model is an actual representation of a "virus" never seen in nature nor observed in the fluids of a sick host would not pass scientific muster. However, this age of molecular and digital trickery is exactly where we are heading currently if we allow those in charge to lead us down this false path.

One of the people promoting these fraudulent activities is Steve Kircsh. Mr. Kirsch is a serial entrepreneur and a Silicon Valley philanthropist who invented the optical mouse and one of the earliest search engines known as Infoseek. He has a BS/MS in Electrical Engineering and Computer Science from MIT. Mr. Kirsch founded the COVID-19 Early Treatment Fund (CETF) which funded early research into drugs such as fluvoxamine to treat "Covid" patients. He is also Executive Director of the Vaccine Safety Research Foundation (vacsafety.org) which is meant to research the safety of the "Covid" vaccines. This is how the VSRF mission statement describes the organization:

"The primary purpose of VSRF is to advance scientific inquiry as the best way to guide us out of the pandemic. We present the most up-to-date and relevant information on COVID-19 policies, free from corporate press, agenda-driven narratives, and sponsorships with conflicts of interest. We encourage questions and an open dialogue of transparency on any medical and scientific information presented."

https://www.vacsafety.org/about

Mr. Kirsch's organization states that its primary mission is to advance scientific inquiry and that it encourages questions and an open-dialogue regarding scientific information. Thus, it is quite confusing that Mr. Kirsch is seemingly against both of these defining principles of his organization.

We recently reached out to Steve in order to see if he would be willing to lend his support to a challenge intending to end the "virus existence" debate once and for all. Knowing full well that Steve believes in the existence of "viruses" based on the opinions of his own experts, we had high hopes that scientific curiosity would win out. We had hoped that he would be willing to meet us halfway and that he would accept the offer to see if the methods used by virologists to prove the existence of "viruses" were actually valid when put through proper scientific protocols with proper controls. For those who are unfamiliar with the proposed challenge, you can find the details here.

Unfortunately Steve declined the offer to sign on as a signatory which is absolutely fine as we knew that many of those who cling to the "virus" story would be unwilling to be associated with a challenge looking to prove that these entities do not exist. Steve's lack of participation was not unexpected to say the least. However, what was unexpected was to see Steve write a misleading hit-piece about the challenge and those who reached out to him.

Sadly, this is not the first time that I have felt compelled to respond to false and misleading information coming from Steve Kirsch. I would rather not give the man any more of my time as I feel he is attempting to divide and distract. I've previously addressed his inaccurate claims on isolation and purification in order to set the record straight and I had hoped that would be the end of it. However, after reading his latest post that was sent to me, it became clear that there are once again misrepresentations and illogical leaps being bandied about as if they are facts which are in need of being addressed.

In his blog post titled Settling the virus debate challenge from Dr. Sam Bailey, Steve attempted to make the case as to why the challenge to virology that was presented to him was unacceptable. Steve did so by doing what he does best: making excuses, misrepresenting the facts, and hiding behind others who do the thinking for him. In order to clear things up, let's go through Steve's claims one by one and see if they hold up.

Here are the details according to Steve:

"I requested a debate with Christine's team, but Christine wrote she was too busy to reply at the time. Now she wrote to me that she won't debate me."

While I won't completely touch on this as I was not directly involved in the conversations, let me assure you that Steve is being misleading. Christine Massey will be releasing full details of their most recent exchanges in the near future. For those who do not know Christine, she has been amassing a collection of vitally important Freedom of Information (FOI) requests from many institutions stating that they have no studies or records of purified/isolated "SARS-COV-2" as well as many other "viruses." Regarding the debates that Steve has proposed, she has consistently shown that Steve will claim one thing in a private email thread while incorrectly recounting said events to his audience. In the past, he stated that Christine was unwilling to debate him after he demanded a 5 hour Zoom call between Christine by herself and his own team of experts (whom he refused to name).

A 5 hour Zoom call?!?!

While Christine has proven herself a capable debater in her own right, requiring a 3-on-1 five-hour marathon was an unfair proposal. Christine reached out to Dr. Andrew Kaufman, Dr. Tom Cowan, Dr. Mark and Sam Bailey, and others to participate along with her in a debate between Steve and his unnamed experts. It got to the point where Dr. Kaufman was in contact with Steve and even wrote out a debate proposal:

Debate question:
The published experiments on the isolation and in silico genome sequencing prove the existence of the SARS-CoV-2 "virus." True or False?

The purpose of this debate is to engage in a healthy scientific discussion. The spirit and philosophy of scientific inquiry demands attempting to refute all theories until it is clear they are irrefutable. This debate rekindles that spirit and serves to advance the state of truthful knowledge about the natural world. As such, the debate must only include scientific arguments. The focus is on the experimental procedures used to allege the existence of viruses, in particular SARS-CoV-2. Have these methods demonstrated the existence of a real biological entity found in nature or are they a misinterpretation resulting from the experimental procedure itself? Why have virologists been unable to extract and purify viral particles directly from the host? Why do they rely on computer computation to construct a genome? Have proper control experiments been done? If not, why?)

In the end, Steve was the one who called everything off in a blog post as he felt that the debate challenge he initially offered was now somehow a waste of his own time and he instead left it to his readers to debate Christine's team for him:

Why spend time educating yourself on the "virus" isolation topic you consistently write about as if you understand it? Let's think about this for a minute… 🤔

You can see some of the exchange here.

Steve demanding an answer to his question before being willing to debate. This looks familiar. 🤔

"Richard Fleming requested a debate with them as well and they wouldn't debate him either."

According to Steve, we won't debate Richard Fleming. Why wouldn't anyone want to participate in a debate with Richard Fleming? Could it be that, when Fleming agrees to a civil discussion ahead of time, he completely disregards his previous pre-debate agreement on the air and launches into numerous ad hominem attacks and rudely interrupts his opponent as seen in his exchanges with Dr. Robert O. Young?

Interestingly, myself and others got into a post-debate debate with Fleming in the comments of the video when it was originally released. Sadly, Fleming deleted his comments afterwards in order to cover up all of the evidence. He has a bad habit of doing such a thing as shown in the comments section of this page.

Debate, delete, and run. Not a very admirable debate tactic.

There are other reasons for why those who know of Fleming do not wish to engage with him but I will let them slide for now. The bottom line is that Fleming is not an honorable man when it comes to debates. Character counts Steve.

"I asked Christine, "OK, so if it isn't a virus, explain to me what my wife caught from her golfing friend who had COVID, and what I caught from my wife. If it wasn't the COVID virus, then what the heck was it? The COVID tests were positive for all of us after we got symptoms." Every email, Christine avoided answering my question. So I had to ask several times! Finally, she wrote the following: "Steve, I sent you the challenge and now you insist on diverting the conversation to your wife and asking what covid is and what people (who I have zero direct knowledge of) allegedly caught.  We all know what covid is claimed to be and what people think they "caught"." So she was being evasive and her answer to my simple question is evasive once again! This is important. They cannot answer this simple question. It is their Achilles heel. They like to claim that the virus doesn't exist, but they cannot explain what COVID is if it isn't a virus, nor do they have a set of tests to PROVE that THEIR theory of what it actually is is correct. Watch this video at 1:47:19. Why aren't THEY spending the money to prove THEIR theory? Gotta wonder about that one. The point is this: If they cannot PROVE their alternative hypothesis then why should the demand proof of the current hypothesis? I've emailed Tom Cowan directly and he said he didn't know what I had. I got "it" from my wife for sure."

Steve is engaging in a few logical fallacies here. Shocking, I know. Steve wants us to explain how he and his wife got sick if it wasn't "SARS-COV-2." This is a logical fallacy known as affirming the consequent. This is a logical error that assumes that if the consequent is said to be true, then the antecedent is said to be true as a result. It is normally expressed like this:

If X then Y.

Y.

Therefore X.

Or in this case: If there is a "virus," I will get sick. I got sick, therefore there is a "virus."

Steve also wants us to explain how both he and his wife got sick around the same time and tested positive for a "virus" using tests repeatedly shown to be inaccurate and fraudulent. This is called a false cause fallacy which is where it is presumed that some sort of perceived relationship between two things means that one caused the other. Just because Steve and his wife became ill around the same time does not mean that a "virus" was transferred between them. Just because they both tested positive on fraudulent tests does not mean a "virus" was detected. There are many proven reasons for why people can become ill:

We can not determine what caused Steve nor his wife to become ill. That would require examining numerous factors both physical and mental which is beyond our capabilities.

Steve also seems to believe that we must provide him an alternative hypothesis and prove it in order to reject the current one. This is also untrue as there is no requirement that one must provide an alternative when critiquing the current dogma. In fact, none of us are providing an alternative hypothesis so there is nothing for us to prove. Steve is simply engaging in a third logical fallacy which is shifting the burden of proof. As Steve and Co. are the ones making the claim that "viruses" exist, the onus is on them to back up their assertion with evidence proving this existence.

"It's not cheap to do the tests they are requesting and they won't pay the costs. They claim they have some pledges available of $500K, but pledges are not the same as cash on hand (I'm an expert on that one). They basically insist that rich people like me should spend our money to prove their hypothesis."

This is blatantly false as it was never insisted that Steve needs to pay to prove our "hypothesis." The challenge is meant for testing their hypothesis that "viruses" exist and cause disease by performing the proper controls that should have been performed by virologists from the very beginning. Steve was only asked to either agree or disagree to supporting a proposal involving independent labs performing the proper scientific validation for his hypothesis. He obviously declined.

"If they have an alternate hypothesis on what is causing people to all come down with a respiratory infection that is so severe they have to go to a hospital, I'm all ears. But they have none. I suspect their purpose is to distract us from the main vaccine narrative. If they want to fund the research they want, we are happy to do it."

Again, we do not need to supply an alternative hypothesis as to what is causing disease in order to disprove the current one. There are numerous factors which can cause disease. Regarding respiratory disease, Steve is conveniently ignoring the increasing air pollution problem as a major factor. However, it is not the only factor. What Steve and Co. want people to believe is that there is one cause (i.e. "SARS-COV-2") that is resulting in a "new" disease which, oddly enough, just so happens to have no new or specific symptoms. He wants his audience to believe in the "Covid" lie and to trust the science and the evidence already presented. We have repeatedly challenged said evidence and we are now seeking to hold them accountable to show that the methods used in these studies are indeed valid. It is very telling that they want no part in performing proper scientific validation.

"This is not my field of expertise at all. I rely on other people around me who I trust. These people are all red-pilled with respect to the vaccine. It is possible that they are blue pilled with respect to the virus, but generally red-pilled people are red-pilled in many areas. None of them found the hypothesis compelling."

Steve has a habit of reminding his readers that his experts do the thinking for him. It is odd that he continues to insist on writing about a topic that he does not understand.

"There is a video of Purnima Wagh (full videohighlights) who says she had $1.5M to do the isolation work and they found nothing. They said in the video that the CDC wouldn't send them a sample. This is very interesting. But you can buy SARS-CoV-2 samples commercially from a number of commercial suppliers including ATCC. Sin Lee bought his reference from Boca Biolistics Reference Laboratory, Pompano Beach, FL. The samples cost under $2K. Why didn't they do that? My colleagues (such as Sabine Hazan's lab) have bought these samples and they matched the gene sequences from their infected patients. If the virus doesn't exist, how do they explain that? And how can you explain Sin Lee's papers (see below)? If the virus doesn't exist, then how do you explain his results? We'd be DELIGHTED to debate Purnima Wagh. I've emailed her and have not heard back."

You can not buy purified and isolated particles claimed to be "SARS-COV-2" which comes directly from the fluids of a sick human but you can purchase lab-created cell-cultured concoctions said to contain the fictitious entity known as "SARS-COV-2." Steve doesn't understand purification and isolation which is why he believes that buying commercially made cell-cultured goo is acceptable. If you would like to understand why cell cultures are invalid, please see this article.

As for genome sequencing, Steve is trying to distract with indirect evidence. As he knows that they can not provide direct evidence of purified/isolated particles taken from the fluids of sick humans which were proven pathogenic in a natural way, he is opting for the latest and greatest indirect evidence to bamboozle his audience with. However, what Steve fails to understand is that in order for the original "SARS-COV-2" genome (which all others are based upon) to be considered an accurate representation of a "virus," the "virus" must be shown to exist in a purified/isolated state first in order to be sequenced properly. Otherwise, a whole range of substances are sequenced along with the assumed "virus" including host DNA, bacteria, fungus, extracellular vesicles, etc. If cultured, you have added foreign animal DNA from the cell line as well as the fetal bovine serum used as the medium. The original "SARS-COV-2" genome is a fraudulent assembly stemming from the unpurified BALF of one patient. Every other genome has been built upon this erroneous foundation.

And for the record Steve, you spelled Poornima (not Purnima) Wagh's name wrong which may be why you haven't heard back as you potentially e-mailed the wrong woman.

"Their challenge to prove there is a virus was accepted by Dr. Kevin W. McCairn, who created a web page accepting the challenge and asking them to put up the money to pay for the tests they wanted. Now, for some odd reason, they do not accept the offer that they asked for."

There is quite a bit wrong with Steve's claims here. First of all, had McCairn actually read the challenge, he would have noticed this statement:

STEP ONE
5 virology labs worldwide would participate in this experiment and None would know the identities of the other participating labs"

By McCairn publicly announcing his acceptance to participate in the challenge rather than doing so privately, he disqualified himself from being able to be a participant. I notified him of this under both of the comments he had left on my blog.

Interestingly, based on McCairn's acceptance statement, he seems to agree with us that the proper scientific validation studies have not been performed:

"I have seen your video asking for laboratories to test the underlying assumptions regarding virology.

I have, available to me, all the laboratory facilities and animal facilities required to perform these experiments."

"I believe that you will not accept the offer of lab facilities or put forward the money to fund such studies. I have publicly sent this email so people will know if you are lying about your intentions to engage in a proper scientific investigation."

It appears rather clearly that McCairn is admitting that the proper scientific investigation testing the underlying assumptions of virology have never been carried out. He offered to do the proper scientific investigation we are seeking thus admitting that the investigations up to this point have been neither proper nor scientific. This is exactly our point as none of the virology studies adhere to the scientific method and are therefore by definition pseudoscience.

Beyond McCairn publicly disqualifying himself, he has consistently shown in the past to be disrespectful while making disgusting comments about Dr. Sam Bailey as well as being prone to resorting to ad hominem attacks. This behavior can be seen on full display in a recent debate with Dr. Mark Bailey:

McCairn's disrespectful and disgusting behavior can also be seen in this recent email exchange with Christine Massey:

Once again Steve, character counts and you should understand why we do not want to associate with McCairn based on his repeated pattern of inappropriate behavior.

"When McCairn pointed out that the challenge was accepted and the originators then didn't reply, Christine ostensibly threatened McCairn with legal action. You really can't make this stuff up. Here's the actual email exchange with McCairn's acceptance and also a debate offer from Dr. Fleming."

As I stated previously, this is a flat out lie that no one responded to McCairn. I replied to McCairn letting him know that he had disqualified himself by announcing publically his intended participation. Obviously, this would defeat the purpose of blinding the labs to each other if they all announce their acceptance to the world. However, McCairn never responded back to me for some reason:

"Now of course, they will then tell their followers that McCairn, Fleming, and I are all bad people and they don't want to waste their time with us."

We allow people to judge you all based upon your responses and your actions. To anyone looking at the exchanges any of us have had with Fleming and McCairn, it is fairly obvious why we do not wish to engage with either of them again. In regards to Steve, he was approached to sign on as a signatory as a interested party willing to see how this challenge worked out. There was no financial requirement for him to do so. It was all in the interest of both sides coming together halfway in order to see the proper scientific validation and control experiments carried out. However, Steve declined and decided to try and change the narrative to the "No Virus" side being unwilling to debate his "experts."

This was never about a debate Steve. This is about proving whether or not the methods used by virologists are valid and that the particles assumed to be "viruses" exist as sold. One must wonder why you have no interest in seeing this process play out.

From Sin Lee confirming the lack of accuracy of the PCR test

He wrote me:

The PCR tests for COVID-19 have at least 40% false positive rates and an unknown % of false negatives. The antigen tests may work when the viral loads are very high. But even the CDC has publicly advised that all antigen positive cases be retested by PCR. 

The PCR test kits at best have 42% false positive rates as I reported in this preprint manuscript: https://www.preprints.org/manuscript/202204.0091/v1

Oddly enough, it appears we have an area that we can all somewhat agree on. PCR test results are inaccurate. While Sin Lee gives them at best a 42% false-positive rate, the true number is actually 100% false-positive rate as no PCR test has ever been calibrated and validated against purified and isolated particles assumed to be "viruses:"

This is from the FDA emergency use authorization of the CDC's PCR test used in the USA:

"Since no quantified virus isolates of the 2019-nCoV were available for CDC use at the time the test was developed and this study conducted, assays designed for detection of the 2019-nCoV RNA were tested with characterized stocks of in vitro transcribed full length RNA (N gene; GenBank accession: MN908947.2) of known titer (RNA copies/µL) spiked into a diluent consisting of a suspension of human A549 cells and viral transport medium (VTM) to mimic clinical specimen."

https://www.fda.gov/media/134922/download

From the Drosten PCR Test used around the world:

"The ongoing outbreak of the recently emerged novel coronavirus (2019-nCoV) poses a challenge for public health laboratories as virus isolates are unavailable while there is growing evidence that the outbreak is more widespread than initially thought, and international spread through travellers does already occur."

"We aimed to develop and deploy robust diagnostic methodology for use in public health laboratory settings without having virus material available."

"In the present case of 2019-nCoV, virus isolates or samples from infected patients have so far not become available to the international public health community. We report here on the establishment and validation of a diagnostic workflow for 2019-nCoV screening and specific confirmation, designed in absence of available virus isolates or original patient specimens. Design and validation were enabled by the close genetic relatedness to the 2003 SARS-CoV, and aided by the use of synthetic nucleic acid technology."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6988269/

Thus, all results from the tests are absolutely meaningless. There are many other reasons why PCR is inaccurate, from the prevalence problem to the issues of contamination, all of which can be found here.

"I asked him directly, is the virus real? He wrote back:

Of course, the virus is real. 

Sanger sequencing electropherograms do not come out of thin air. It is the genetic fingerprint of the virus.

Sanger sequencing is the gold standard for confirming the presence of the virus."

Apparently, if Steve asks Dr. Sin Hang Lee, a pathologist and director of Conneticut's Milford Molecular Diagnostics Laboratory, if a "virus" is real and the Dr. answers "yes," it is case closed. Of course, both Steve and Dr. Lee want you to believe that A,C,T,G's in a computer database is all the evidence that is needed in order to prove the existence of a "virus." No purified and isolated "virus" is necessary if the computer assembles a theoretical genome of an invisible entity. They will tell you PCR is inaccurate but in the same breath tell you Sanger sequencing of unpurifued samples is the "gold standard" to confirm the presence of a "virus."

However, is Sanger sequencing the "gold standard" or is it NAAT's?

"The "gold standard" for clinical diagnostic detection of SARS-CoV-2 remains laboratory-based (moderate- and high-complexity) NAATs."

https://www.cdc.gov/coronavirus/2019-ncov/lab/resources/antigen-tests-guidelines.html

Or is the gold standard "viral" culturing?

"During our Open Evidence Review of oral-fecal transmission of Covid-19, we noticed how few studies had attempted or reported culturing live SARS-CoV-2 virus from human samples.

This surprised us, as viral culture is regarded as a gold standard or reference test against which any diagnostic index test for viruses must be measured and calibrated, to understand the predictive properties of that test. In viral culture, viruses are injected in the laboratory cell lines to see if they cause cell damage and death, thus releasing a whole set of new viruses that can go on to infect other cells."

Are you infectious if you have a positive PCR test result for COVID-19?

So many "gold standards" to choose from, so little time. However, without purified and isolated particles proven to be pathogenic, there is no standard. It amounts to nothing more than:

"When I press these folks on why any given study doesn't meet their standards, I don't get technical rebuttals. I get "Gates funded it" or "Fauci funded it" types of answers which dismiss most of the evidence we have unfortunately. [i.e., they dismiss our evidence not for technical reasons, but based on who funded the research]"

The above section is quoted from one of Steve's anonymous experts. If he/she is not getting technical rebuttals, he/she is not talking to the right people. Perhaps Steve's anonymous expert would like to reach out to any of the signatories on the challenge for a technical rebuttal that does not involve Gates and Fauci? I assure you, we exist. All you have to do is contact us.

Sin Lee's challenge

Sin wrote:

Tom Cowan claimed the virus has not been isolated. But the virus has been isolated by the CDC and marketed by ATCC as the control materials. I bought the virus as the control for my CLIA tests. Many others do.

I know others that use the ATCC materials and they work as expected. If the virus doesn't exist, then how is that possible? Also, ATCC wouldn't be able to sell anything.

Sin also wrote the following challenge which I refer to below as the "Sin Lee challenge":

I have a Preprint manuscript currently under peer review.

There is irrefutable Sanger sequencing evidence that the virus exists and keeps mutating.

If anyone disagrees, please write a critique to challenge my data and interpretation online in the open. I will respond. Other scientists can join in for the debate. 

So if the virus doesn't exist, you simply explain how it is possible he got the results in the paper. Simple.

The Sin Lee Challenge. This is the crux of Steve's article. Instead of joining our proposal and working with us to put the methods of virology to a proper scientific test, Steve and Co. decided to try to change the narrative. They know 100% that they will always lose on the issue of purification and isolation. This was made abundantly clear in Steve's previous article on purification:

"Also, the people I talk to fully acknowledge there is no purified virus, but that it isn't needed because they can do everything they need to do without it. Lanka et al. claim it is needed. So it's now just a matter of opinion. Neither side is going to convince the other side. That's what happened."

"The reason nobody has purified the virus is there is no need to do so in today's world where gene sequencing is readily available."

Steve wants you to believe that the lack of a purified and isolated "virus" is not important:

In place of any actual physical and tangible evidence for the existence of the particles assumed to be "viruses," Steve and Co. want to offer you this instead:

Who needs actual direct proof for the existence of a "virus" when you can have this beautifully crafted arrangement of random A,C,T,G's in a computer database? This kind of "logic" reminds me of a certain scene in Dumb and Dumber:

Steve and Co. want you to believe that genomic sequencing is all that is required in order to prove the existence of a "virus." This is their "irrefutable evidence" as there is no purified and isolated "viral" particles anywhere in Dr. Sin Lee's paper. There are no electron microscopy images of the isolated particles. There is no proof of pathogenicity by subjecting the assumed "viral" particles to a susceptible host recreating the same disease. There is no re-isolation and re-purification of the assumed "viral" particles from the challenged host. There is no independent reproducibility nor replication of the results. There is no adherence to the scientific method. All you will find in this paper, said to be "irrefutable evidence" for the existence of "SARS-COV-2," is data. Period.

It seems that Steve and Co. either ignored or did not heed the warnings of Charles Calisher and 13 other veteran virologists back in 2001:

"Although all that is terrific, says Calisher, a string of DNA letters in a data bank tells little or nothing about how a virus multiplies, which animals carry it, how it makes people sick, or whether antibodies to other viruses might protect against it. Just studying sequences, Calisher says, is "like trying to say whether somebody has bad breath by looking at his fingerprints."

The Old Guard of Virology Warn About the Ways of the New Guard and Their Molecular Toys

Steve and Co. would also do well to read this informative 2015 paper by Edward R. Dougherty, the Scientific Director of the Center for Bioinformatics and Genomic Systems Engineering, who spoke extensively about the epistemological crisis in genomics and how the accumulation of genomic data is not science:

"High-throughput technologies such as gene-expression microarrays have lead to the accumulation of massive amounts of data, orders of magnitude in excess to what has heretofore been conceivable. But the accumulation of data does not constitute science, nor does the a postiori rational analysis of data."

"Here we focus on how the experimental method leads to a general scientific epistemology and how contemporary genomic research often fails to satisfy the basic requirements of that epistemology, thereby failing to produce valid scientific knowledge."

The Epistemological Crisis in Genomics

Data accumulation is not science. Presenting said data is not "irrefutable evidence" for the existence of an entity never seen in a purified and isolated state. The collection of data does not replace the requirement for evidence that adheres to the scientific method which requires a valid independent variable (i.e. purified/isolated particles) in order to determine cause and effect. It does not matter what Sin's indirect computer-generated evidence shows as it can not take the place of having the necessary direct physical proof. These strings of DNA letters in a data bank tells little or nothing no matter how badly Steve and Co. want to convince you otherwise. For more on why this genomic evidence is invalid, Dr. Mark Bailey wrote an excellent article breaking down the problems with the Sin's paper here.

For a further breakdown of the Sin Lee paper, please watch this Dr. Tom Cowan webinar recorded 7/27/22:

https://viroliegy.com/2022/07/28/a-follow-up-to-the-virus-challenge-7-27-22-dr-tom-cowan-webinar-with-dr-andrew-kaufman-mike-stone-and-mike-donio/

Fraudulent foundation.

While the illogical claim that genomic data is somehow "irrefutable evidence" of a "virus" is bad enough, there is an even larger issue lurking underneath the surface here that needs addressing. Why are Steve and Co. relying on a non-peer-reviewed preprint study from June 2022 as their "irrefutable evidence" to begin with? Shouldn't the "irrefutable evidence" for the existence of "SARS-COV-2" come from the initial "virus isolation" studies from January 2020 to March 2020?

  1. The Fan Wu Paper (the genome):
  2. The Zhou Paper ("virus" isolation):
  3. The Zhu Paper (first EM images):
  4. The Park Paper (first patient in Korea):
  5. The CDC Paper (first patient in US):

These were the studies that claimed that a new "virus" with a new disease existed. The Fan Wu paper is where the original genome was produced. The Zhou paper has the isolation of the "virus." The Zhu paper is where the original EM images came from. The Park paper is from the first patient in Korea while the CDC paper is from the first patient in the US showing the supposed spread of the "virus." These papers are the foundational evidence presented in the case made before the public for the existence of "SARS-COV-2" yet Steve and Co. did not choose a single one of these as the "irrefutable evidence" for the existence of "SARS-COV-2." Why would that be?

Could it be that because Steve and Co. admit that purification (and therefore isolation) has not taken place, that they already know that they have lost the battle? The physical evidence for the existence of "SARS-COV-2" in and of itself does not exist. It is admitted within these papers by the authors themselves that they can only provide an association yet not proof that "SARS-COV-2" causes disease due to a small sample size as well as the inability to fullfill Koch's Postulates, the very criteria needed to be met in order to prove a disease-causing pathogen exists:

Fan Wu:

"Although the isolation of the virus from only a single patient is not sufficient to conclude that it caused these respiratory symptoms, our findings have been independently corroborated in further patients in a separate study29."

Zhou:

"The association between 2019-nCoV and the disease has not been verified by animal experiments to fulfil the Koch's postulates to establish a causative relationship between a microorganism and a disease. We do not yet know the transmission routine of this virus among hosts."

Zhu:

"Although our study does not fulfill Koch's postulates, our analyses provide evidence implicating 2019-nCoV in the Wuhan outbreak. Additional evidence to confirm the etiologic significance of 2019-nCoV in the Wuhan outbreak include identification of a 2019-nCoV antigen in the lung tissue of patients by immunohistochemical analysis, detection of IgM and IgG antiviral antibodies in the serum samples from a patient at two time points to demonstrate seroconversion, and animal (monkey) experiments to provide evidence of pathogenicity."

Many of the authors of these early studies also admitted to not purifying their "viruses:"

No Purification = No Isolation.

If the foundational papers supplied as evidence for "SARS-COV-2" are not "irrefutable evidence" for the existence of "SARS-COV-2," this means that the case for the existence of this "virus" was built upon a faulty and fraudulent foundation. As all other studies that have been conducted since are built upon this same faulty and fraudulent foundation, this means that they too share this very designation, including Dr. Sin Hang Lee's paper which relied on previous fraudulent genomic data to produce his own results. Steve and Co.'s "irrefutable evidence" is not scientific evidence for the existence of "SARS-COV-2" at all. It's nothing but genomic data.

"I told him we are interested in resolving the issue as well so we can put it to bed, and suggested we collaborate on defining the challenge. A challenge defined by parties on both sides is what you want if you want to convince the other side.

He wrote back:

Hi Steve, the challenge is clear, simple and doable, if any of these folks have specific requests or questions about the full protocol which is to come, please have them send them to us.   There is no need to proceed in the stepwise manner you suggest.   All the best, Tom

That didn't sound like someone who is interested in collaborating with others to find out what the truth is."

I'm not sure what the full context of this exchange was and I'm not even sure what to make of it here based on this single snippet. It seems Steve wants to collaborate. Great, this is the reason we reached out to him. Dr. Cowan responded to Steve by telling him to send specific requests and questions about the full protocol (which is undecided and yet to be put together) to us in order for them to be addressed. The "action of working with someone to produce or create something" is the very essence of collaborating. How is Dr. Cowan's response not in lockstep with that? Steve wants you to believe that we are unwilling to work together, which is obviously not the case at all.

"We are claiming the virus exists which is different that has it been isolated based on YOUR definition of isolated. Different people have different definitions of what that term "isolation" means in virology, as I'm sure you must be aware of."

Steve is really having a hard time understanding and grasping the meaning of the word isolation, even though I already explained it to him previously. Once again, for old time's sake:

Isolation

1the state of being in a place or situation that is separate from others: the condition of being isolated

2the act of separating something from other thingsthe act of isolating something

https://www.merriam-webster.com/dictionary/isolation
Isolate

1: to set apart from others

2to select from among others especiallyto separate from another substance so as to obtain pure or in a free state

https://www.merriam-webster.com/dictionary/isolate

There is no "OUR" definition of isolation/isolate. There is only THE definition for isolation/isolate. If Steve is going to claim that virologists get to make up their own definition which is the complete opposite of the accepted definitions for these words, he must show who determined this definition change, why it is valid, and where in any dictionary the term isolation/isolate means the mixing of many substances together in a culture.

"Here's one of their products for SARS-CoV-2. Note the world "isolated." It is the RNA that is isolated, not "the virus." This doesn't mean that that the virus doesn't exist. If the virus didn't exist, they wouldn't be able to sell the isolated RNA of the virus."

Here, once again, Steve is trying to fool you with genomics. According to his thought process, if a manufacturer claims it is selling you "viral RNA," the "virus" must exist. Manufacturers can not just sell you something that doesn't exist, correct? Well, companies definitely can sell you something that doesn't exist such as a plot of land on the moon or naming a star after a loved one. Obviously, these are gimmicks that play on people's emotions.

As far as "viral" RNA is concerned, these companies are selling lab-created cell cultured concoctions with the claim that "viral" RNA exists within it. Interestingly, they do not stand by the accuracy of any claims, as noted in the product sheet for the "viral" RNA product Steve supplied:

"While ATCC uses reasonable efforts to include accurate and up-to-date information on this product sheet, ATCC makes no warranties or representations as to its accuracy. Citations from scientific literature and patents are provided for informational purposes only. ATCC does not warrant that such information has been confirmed to be accurate or complete and the customer bears the sole responsibility of confirming the accuracy and completeness of any such information."

https://www.atcc.org/api/pdf/product-sheet?id=VR-3347D

As previously explained, "SARS-COV-2" has never been scientifically proven to exist in a purified and isolated state. As the assumed "viral" RNA comes from an unpurifued cell-cultured source that contained many other host and foreign genetic materials used in its creation, there is no evidence that the RNA comes from a "virus" whatsoever. In fact, all "viral" RNA and sequences are most likely nothing more than a mixture of human, animal, bacterial, fungal, and other unknown sources of genetic material. These mixtures of RNA are claimed as "viral" and added to a database in order to build a "viral" library. There is no evidence whatsoever that any RNA ever came from any "virus."

"However, the bet was overturned on appeal not because the virus was proven not to exist, but because Lanka cleverly specified the challenge as "a SINGLE paper."

"The bet was disingenuous. If Lanka really wanted to answer the scientific question about measles, then why the single paper limitation? That's not how science works. If the existence and size measurement is covered in six papers, why is that not sufficient? As far as I know, there is no "single paper" requirement of science to prove anything."

While I will not go in depth on the measles "virus" trial as it has been covered extensively in many other places, especially this excellent breakdown by Feli Popescu, I will point out a few things. First, these are the six papers supplied by David Bardens:

1. Enders JF, Peebles TC. Propagation in tissue cultures of cytopathogenic agents from patients with measles. Proc Soc Exp Biol Med. 1954 Jun;86(2):277–286.

2. Bech V, Magnus Pv. Studies on measles virus in monkey kidney tissue cultures. Acta Pathol Microbiol Scand. 1959; 42(1): 75–85

3. Horikami SM, Moyer SA. Structure, Transcription, and Replication of Measles Virus. Curr Top Microbiol Immunol. 1995; 191: 35–50.

4. Nakai M, Imagawa DT. Electron microscopy of measles virus replication. J Virol. 1969 Feb; 3(2): 187–97.

5. Lund GA, Tyrell, DL, Bradley RD, Scraba DG. The molecular length of measles virus RNA and the structural organization of measles nucleocapsids. J Gen Virol. 1984 Sep;65 (Pt 9):1535–42.

6. Daikoku E, Morita C, Kohno T, Sano K. Analysis of Morphology and Infectivity of Measles Virus Particles. Bulletin of the Osaka Medical College. 2007; 53(2): 107–14.

As can be seen, we have papers from over the course of six decades. The first, from John Franklin Enders in 1954, is the original publication claiming the isolation of the measles "virus" and it established the cell culture techniques still in use by virologists today. Thus, all other papers supplied were built upon the foundation of this single paper. Yet, the court decided that NONE of these papers, even the original Enders paper claiming the proof for the isolation of the measles "virus," was sufficient as evidence alone that the measles "virus" exists. In other words, the very paper claiming the existence and isolation of the measles "virus" was not "irrefutable proof" and could not win a court case. Let that sink in.

Interestingly, even though Steve is claiming that the single paper limitation is not how science works, he is standing by a single June 2022 paper from Dr. Sin Hang Lee as his "irrefutable evidence" for the existence of "SARS-COV-2." That seems rather hypocritical Steve, don't you think?

"The fastest way to settle this is a debate. Otherwise, we'll be waiting about a year for the challenge to complete (assuming they can raise the $1M required to fund the challenge)."

If you are qualified to discuss the topic (e.g., you have read and understand Sin Lee's papers cited above and can explain to us how he goofed in your application since he thinks the virus exists), we'll have the debate. Simply provide a scientifically plausible hypothesis explaining his observations. If it wasn't a virus he sequenced, what was it? Or conversely, in your lab if you proved the samples from ATCC do not contain parts of the the SARS-CoV-2 genome as advertised, show us evidence of that.

Alternatively, simply show us your CDC 0728 permit and proof you work there (e.g., use your work email address)."

Steve and Co. will debate you…but only if you have the proper "unique" credentials as well as a scientific hypothesis and refutation of Dr. Sin Lee's paper that they will accept. You must also have a social media following it appears:

If you believe either:

  1. SARS-CoV-2 virus doesn't exist
  2. viruses in general don't exist

then I challenge you to a $1M bet.

If you are confident you got it right, you should jump at the chance to double your money. If you don't have $1M, do a fundraiser and tell people this is a slam dunk and it's a great way for them to double their money. After all, if you are right, you should have PLENTY of people who believe in you since you represent the truth.

While I was finishing up this article, Steve decided to add more fuel to the fire by challenging those of us who released the Debunking the Nonsense presentation to a $1 million dollar debate challenge. He also wrote his own article on his blog about his latest attempt to divert and distract from the No "Virus" Challenge he was presented with that is intended to either validate or invalidate the methods used by virologists. This trick by Steve and Co. is designed to make those of us challenging virology look like we are not confident in our position if we decline his one million dollar offer. However, it should be fairly clear that none of us have a cool million dollars lying around just in case we are challenged to a debate by millionaires. Steve might as well have have offered us this:

As I said previously, Steve and Co. are not interested in validating the methods of virology scientifically. They are interested in changing the narrative as quickly as possible to a debate, an area that they feel they have a tactical advantage on for some strange reason. However, a debate is not in the spirit of collaboration and comraderie. A debate does not settle the question as to whether or not the methods of virology are valid. A debate does not determine the existence of a replication-competent intracellular parasite transferring from person-to-person causing the same exact disease. The time for debating is over. Even past Steve agreed that debating is a pointless endeavor:

"That us why debating Kaufman and his collaborators is fruitless: each side will dig in on their own definitions and settle nothing."

https://stevekirsch.substack.com/p/has-the-virus-been-isolated-yes?fbclid=IwAR14YOf73MLPEa34XXu5oGL4lZmnOYZnPCN6li8rhcmPIYwdbRomJB3IAV4

"People have asked me to debate whether the virus has been isolated. I'm not willing to invest my time in this debate because it's off topic for me and doesn't advance my agenda. If I win, nothing changes. If I lose, nothing changes. Why would I spend time educating myself in this area to achieve nothing?"

https://stevekirsch.substack.com/p/does-anyone-want-to-debate-does-the

It is time to perform the proper scientific experiments which adhere to the scientific method with valid controls. This is the only way this gets settled.

In Summary:
  • Steve Kirsch was offered the chance to collaborate and participate in the "No Virus"challenge yet he declined
  • Steve claimed that Christine Massey would not debate him which was never the intention for any of us for reaching out to him about this challenge in the first place
  • Steve claimed that we would not debate Richard Fleming, a man who has shown himself to be a dishonorable debater in the past
  • Steve engaged in at least 3 logical fallacies trying to get us to explain to him how and why both he and his wife did not get sick from a "virus"
    1. Affirming the consequent
    2. False cause
    3. Burden of proof
  • Steve claimed that we were not willing to debate Kevin McCairn, another man who has shown himself to be dishonorable in debates and who has engaged in disgusting comments directed at both Christine Massey and Dr. Sam Bailey
  • Steve falsely claimed that none of us responded to McCairn's acceptance even though I had told McCairn he had disqualified himself by publicy announcing his intention as the goal is for the labs to be blinded to each other
  • There is some area of agreement between all of us as we all seem to agree that the PCR tests are inaccuate
  • Steve and Dr. Sin Lee proposed the Sin Lee Challenge as a way to distract from the "No Virus" challenge as well making it as a requirement to debate
  • Steve wants you to forget about the required evidence of purified/isolated "virus" which he and his experts admitted did not exist in the past in order to believe that Sin's genomic data is "irrefutable evidence" for the existence of "SARS-COV-2"
  • In 2001, virologist Charles Calisher, along with 13 other veteran virologists, warned that a string of DNA letters in a data bank tells little or nothing and just studying sequences is "like trying to say whether somebody has bad breath by looking at his fingerprints."
  • In 2015, Edward R. Dougherty, the Scientific Director of the Center for Bioinformatics and Genomic Systems Engineering, wrote a paper stating that the accumulation of data does not constitute science, nor does the a postiori rational analysis of data and that contemporary genomic research often fails to satisfy the basic requirements of that epistemology, thereby failing to produce valid scientific knowledge
  • Steve wants you to believe that Sin's pre-print non-peer-reviewed paper published in June 2022 is "irrefutable evidence" even though it lacks:
    1. Purified and isolated "viral" particles
    2. EM images of the particles
    3. Proof of pathogenicity
    4. Reproducibility and replication
    5. Proper controls
  • Meanwhile, Steve and Co. failed to offer any of the original "SARS-COV-2" studies presented from January to March 2020 as their "irrefutable evidence"
  • These papers include:
    1. The Fan Wu Paper (the genome)
    2. The Zhou Paper ("virus" isolation)
    3. The Zhu Paper (first EM images)
    4. The Park Paper (first patient in Korea)
    5. The CDC Paper (first patient in US)
  • Some of the author's of these papers admitted to not fulfilling Koch's Postulates, the very criteria needed to be met in order to prove a new pathogen causing disease exists, while others admitted to not purifying the "virus"
  • Sin's studies and all others that came after those originals are built from the false and fraudulent foundations of these original publications
  • Steve attenpted to make the case that Dr. Cowan did not want to collaborate even though Dr. Cowan asked Steve to send specific requests and questions about the full protocol (which is undecided and yet to be put together) to us in order for them to be addressed
  • Steve is still under the impression that isolation means the combination of many elements together
  • Steve is also under the belief that if a company claims it is selling "viral" RNA, this is proof that they are selling "viral" RNA, even though the company cited by Steve admits that it will not back the accuracy of any of its claims about its products
  • Steve attempted to claim that the Dr. Lanka's measles trial was disingenuous as Dr. Lanka asked for a single paper to be provided as evidence which Steve claims is not scientific
  • Steve then hypocritically challenged anyone to refute Sin Lee's SINGLE paper he claims as "irrefutable evidence" for the existence of "SARS-COV-2" as a requirement to debate his experts
  • If you want to debate Steve, you must also have the proper "unique" credentials as well as a social media following, thus showing that Steve is failing to live up to the promise he set for his organization to encourage questions and an open dialogue of transparency on any medical and scientific information presented

As I said before, it was not my intention to ever respond to another Steve Kirsch article. He has consistently shown me that he does not understand the very topic he is writing about. This is not just my own assessment as it is even admitted by Steve publically that it is his experts feeding him his information (as well as apparently his opinion) as Steve is no expert himself. However, I was holding out hope that a man of science would be interested in actually participating in a challenge designed to perform the proper scientific validation irregardless of the outcome. I had hoped Steve would see the value in putting aside any differences and to work with us in a joint effort to see what the science truly shows when performed as closely to the scientific method as possible. Steve has shown interest in the past in actually funding and performing independent research:

So it's up to us if we want answers

"Private individuals can fund the needed experiments and have them performed at one of the 10 BSL3 labs in the US.

The cost to do these experiments to show conclusively that the vaccines are both dangerous and ineffective is less than $10M.

I would fund this myself if I had a spare $10M sitting around, but I don't.

And I haven't found a philanthropist in the world who is interested, able, and willing to fund the research."

However, instead of Steve and Co. working with us to get the necessary scientific research performed, we received a declination and a hit-piece. Rather than joining us in a scientific endeavor, Steve would prefer to sit on the sidelines while challenging us to engage in debate with his "experts," a strategy that he has stated in the past is a fruitless waste of time that will change nothing. Steve has decided to counter our efforts to come together by setting forth with a divisive challenge of his own. In order to win this debate, we must agree to his terms. We must tackle his experts and his "irrefutable evidence" made up of genomic data given to him in pre-print form by Dr. Sin Lee. To win, we must defeat the genomic "virus" of Sin.

Let's be very clear. The time for verbal sparring is over and genomic data is not "irrefutable evidence" for the existence of a "virus." These are tactics used by Steve and Co. to distract from the challenge at hand and to change what they see as a losing narrative for their position. If Steve and Co. were truly interested in settling this debate, they would realize that a war of words is not required. Action is. If Steve and Co. were truly interested in science, they would join us in support of carrying out the proper scientific validation and controls. The fact that they declined the offer and would rather carry on with a verbal boxing match should tell you everything that you need to know.

ViroLIEgy
24 Jul 2022 | 2:32 pm

Dissecting “Viruses” and Grapefruits with Eric Coppolino


I recently had the privilege of being on Eric Coppolino's show again to discuss all things virology…and grapefruits! It was a fun conversation where we dove into the recent launch of the No "VIrus" Challenge and some of the issues we continue to see in regards to our current (and potentially future) pandemic(s).

Per Eric:

A pile of dust is not a grapefruit. Mike Stone and Eric Francis deconstruct the notion of a virus.

A grapefruit is not a pile of dust.

"Want a good time? Call up Mike Stone and ask him about viruses. Today we start with understand the Virology Challenge issued by some of your favorite presenters — Mark and Sam Bailey, Tom Cowan, Andy Kaufman and others. Mike is the author of the ViroLIEgy.com website, which should be more famous than it is. In this 50-minute segment, we talk about why you can't sweep the produce department floor and make a grapefruit out of the dust. You're not a bank robber if you have a dollar in your pocket. And a pile of computer code is not a virus. This is an entertaining, no bullshit discussion of what the heck virologists think they are doing. Special cameo by Tony Fauci! He was right in my studio. I made him espresso and we smoked a cigarette for old time's sake."

You can listen to our conversation here:

A pile of dust is not a grapefruit. Mike Stone and Eric Francis deconstruct the notion of a virus.

And please visit Eric's brand new substack for more amazing content!

https://planetwavesfm.substack.com/

ViroLIEgy
22 Jul 2022 | 5:26 am

Debunking the Nonsense


A few months ago, I was invited by Alec Zeck to help develop and participate in a presentation brilliantly led by him and including many other people whom I greatly admire and respect such as Dr. Jordan Grant, Mike Donio, and Jacob Diaz. We set out to create an easy to understand case against the pseudoscience that is virology which can be enjoyed on video as well as read and shared as a slide presentation. We covered many layers of the lie including:

  • The Definition of Isolation
  • A Breakdown of the Methodology
  • Science vs Pseudoscience
  • The Scientific Method
  • The Experts' Excuses
  • The Cell Culture Method
  • The Limitations of Electron Microscopy
  • Misinterpreting EM Images
  • History of the Cell Culture Method
  • The Many Logical Fallacies
  • Stefan Lanka's Control Experiments
  • If Not a "Virus," Then What…?
  • Proof of Contagion?
  • Natural vs Artificial Routes of Infection
  • Why Is This Important?

It has been a long time in the making but the moment has arrived to finally share our work with the world. I hope that you are able to gain some valuable insight from our carefully crafted deconstruction of viroLIEgy. Please share this with as many people as you can so that we can continue to undo the 120+ years of damage that has been done by one of the greatest lies ever sold. Thank you for reading and/or watching!

To download the PDF presentation: https://t.me/debunkingthenonsense/3

To download the PDF presentation for those not on Telegram:

Debunking the Nonsense (1)Download

To download the video presentation: https://we.tl/t-QgvEVJR65f

ViroLIEgy
20 Jul 2022 | 7:03 pm

The Elephant and The Spike


"There is a debate tactic known as 'elephant hurling'. This occurs when the critic throws summary arguments about complex issues to give the impression of weighty evidence, but with an unstated presumption that a large complex of underlying ideas is true, and failing to consider opposing data, usually because they have uncritically accepted the arguments from their own side. We should challenge elephant-hurlers to offer specifics and challenge the underlying assumptions."

Excerpt from Refuting Evolution 2 by Jonathan Sarfati, Ph.D. with Michael Matthews

To those who have looked into virology both critically and logically, it is painfully obvious that there is no scientific evidence for the existence of any so-called "virus." It simply does not exist. This holds equally true for the most recent fictitious boogeyman in "SARS-COV-2." No "virus" has ever been properly purified nor isolated directly from the fluids taken from a sick host and then shown to be pathogenic in a natural way while adhering to the scientific method in order to demonstrate cause and effect. As no "virus" has ever been scientifically proven to exist, it should go without saying that no spike protein said to belong to one has ever met this same criteria either. I recently went through this lack of evidence for the "coronavirus" spike protein here. Thus, it is honestly a waste of time to even entertain the idea of a spike protein until such evidence can be produced for both the "virus" in question and its assumed proteins.

So why am I devoting another article to this 9-12 nm figment of the imagination? I was recently sent a post by Jeremy Hammond titled: Fact Check: COVID-19 Vaccine mRNA and Spike Protein Are Not Cleared 'Within Days' which was supposed to be fact-checking the "fact-checkers." In this article, Mr. Hammond attempted to debunk a "fact-check" by Health Feedback which itself aimed to allay fears about the spike protein causing damage to the body after vaccination. According to "Covid" mythology, the spike protein is claimed to circulate inside the body after mRNA injection. After submitting oneself to the toxic experiment, an unobservable magical process is said to occur where the invisible mRNA puts on its teaching cap and instructs the body on how to create the invisible spike proteins in order to learn how to develop an immune response so that it can fight off the spike protein that it just discovered how to create. Seems like a "beLIEvable" story about the novel "virus," right?

The Health Feedback "fact-check" argued that the spike protein is perfectly safe as it is produced in such small quantities in the body that it is harmless. Mr. Hammond, on the other hand, disagreed with their story and proceeded to provide his own version of events in order to claim that the spike protein by itself is harmful. While it is not my intent to make the case that the Health Feedback "fact-check" is correct (it most definitely is not) nor that the mRNA injections are safe by any means (I have previously shown that they are in fact very harmful with many unknown side effects), I must interject here as Mr. Hammond is attempting to debunk one fictional narrative with yet another, both of which are tied to the existence and supposed pathogenicity of a spike protein.

From what I've been told, Jeremy Hammond is for health freedom and he has a large following. Thus, it is very important that he gets his facts straight so as to not mislead people down a side road right back into the pharmaceutically-endorsed germ theory lie. While I do not know much about him, I have been told that, while he has consistently and rightfully called out the dangers of the vaccines, Mr. Hammond very much pushes the myth that "viruses" exist. That much is clear from his article insinuating that such a thing as a spike protein exists and is by itself pathogenic. Now, it is not my intent to attack Mr. Hammond. Rather, this is an attempt to set the record straight based on the evidence available. Hopefully, this will also stand as a good lesson in always vetting any study before submitting it as evidence to bolster your own argument.

The Elephant Hurl process. 😉

While reading the article, it became clear that Mr. Hammond was using an unsavory tactic to try and debunk the Health Feedback "fact-check." This tactic is known as elephant hurling, which is where one throws out numerous arguments and/or studies in order to create the illusion that the weight of the evidence is on their side. It is an intimidation tactic designed to overwhelm not only the "opponent" (Health Feedback in this case if it were an actual debate) but also those reading the article. It is an attempt to claim that a preponderance of evidence means that one's argument is correct. However, if the preponderance of evidence is based upon a fraudulent foundation, such as the existence of a pathogenic spike protein said to belong to a "coronavirus," the accumulated weight of the evidence is utterly meaningless. What we are left with is a gigantic pile of non-reproducible, non-replicable, and erroneous stories built around a fictional entity. This is very clear after looking at the list of studies supplied by Mr. Hammond.

I have gone through the main studies presented as evidence by Mr. Hammond that a spike protein exists and is pathogenic by itself. I have provided some (not all) of the many faults related to each of these papers. What you will see is that not a single study utilized purified and isolated particles said to be spike proteins. As is normally the case, the researchers engineered their own cell cultured creations claiming the existence of invisible spikes inside the petri dish. The experimental methods attempting to prove pathogenicity relate to indirect observations from 2D and 3D model systems as well as non-specific chemical reactions. In other words, the evidence is entirely in vitro, i.e. created in a lab, and has no bearing on what would or could occur naturally in vivo, i.e. within a living organism. The ensuing breakdown is rather long as Mr. Hammond hurled out quite a few unrelated sources so bear with me and we will get through them all.

The Spike Protein Studies

The Spike Protein Is Not Harmless

"Numerous studies have indicated that the spike protein of SARS‑CoV‑2 by itself, in the absence of whole viable virus, can have pathogenic and toxic effects. The following are some notable examples."

"A study in Neurobiology of Disease in October 2020 found that the spike protein promotes loss of blood-brain barrier integrity and triggers an inflammatory response in brain endothelial cells."

Before diving into this first study, it is extremely important to highlight something critical: not a single one of the proceeding studies submitted as proof of the pathogenicity of the spike protein by Jeremy Hammond use purified and isolated spike proteins from purified and isolated "SARS-COV-2." What is used, instead, is known as a recombinant protein. What exactly is a recombinant protein?

"Recombinant protein is a manipulated form of protein, which is generated in various ways to produce large quantities of proteins, modify gene sequences and manufacture useful commercial products. The formation of recombinant protein is carried out in specialized vehicles known as vectors. Recombinant technology is the process involved in the formation of recombinant protein.

Recombinant Protein is a protein encoded by a gene — recombinant DNA — that has been cloned in a system that supports expression of the gene and translation of messenger RNA (see expression system). Modification of the gene by recombinant DNA technology can lead to expression of a mutant protein. Proteins coexpressed in bacteria will not possess post-translational modifications, e.g. phosphorylation or glycosylation; eukaryotic expression systems are needed for this."

https://portlandpress.com/clinsci/article/136/6/431/231092/SARS-CoV-2-spike-protein-causes-cardiovascular

As can be seen, when discussing recombinant proteins, we are dealing with manipulated substances that are said to have been genetically engineered, modified, and cloned. In order to create the recombinant proteins, an appropriate expression system is needed in order to culture, maintain, and grow the desired amount of proteins for the intended use. These expression systems can come in the form of bacteria, yeast, insects, or mammalian cells.

"In such cases the system in which the protein is expressed must be easy to culture and maintain, grow rapidly, and produce large amounts of protein. Moreover, mammalian proteins also undergo various post-translational modifications. These requirements led to the discovery of protein expression systems. The various protein expression systems are bacteria, yeast, insect or mammalian systems.

The following factors determine the type of expression system used to produce recombinant proteins:

  • time spent in expressing
  • the proteinease of handling
  • the expression system
  • amount of protein needed
  • mass of the protein
  • type of post-translational modifications,
  • number of disulfide bonds
  • destination of the expressed protein

The process of expressing a recombinant protein in an expression system requires the following information/components.

  • identification of the gene that encodes the protein of interest
  • generation of cDNA from the respective mRNA
  • selection of suitable expression vector to insert the gene sequence
  • selection of suitable system that can express the vector
  • appropriate screening and scaling up methods"

https://www.sigmaaldrich.com/US/en/technical-documents/technical-article/protein-biology/protein-expression/protein-expression-systems

Without going into too much detail, it should be clear to see that what these studies are working with are nothing but lab-concocted creations said to contain the invisible spikes that have no relation to what may be theoretically free-floating inside a human body due to "natural infection" with a "virus." There are no purified and isolated spike proteins that are ever observed nor utilized as a valid independent variable in order to determine cause and effect. Thus, any study using recombinant proteins (and/or pseudoviruses as will be seen later) are in fact pseudoscience, i.e. fake science, and should be immediately rejected as a form of valid evidence.

Now, on to Hammond's first study. What you will find is that this study is entirely reliant upon, you guessed it, recombinant spike proteins.

The reagents used for the study included:

  1. "SARS-CoV-2" subunit S1 (RayBiotech, Cat No 230–01101)
  2. "SARS-CoV-2" RBD (RayBiotech, Cat No 230–01102)
  3. "SARS-CoV-2" subunit S2 (RayBiotech, Cat No 230–01103)
    • All three are recombinant "spike proteins" expressed in E. Coli and maintained in a filtered solution in 50 mM Na2HPO4 (pH 7.4), 0.5 M NaCl, 450 mM imidazole, and 6 M urea.
  4. "SARS-CoV-2 S1" (RayBiotech, Cat No 230–30161-10)
    • A recombinant "spike protein" grown in Human embryonic kidney 293 (HEK293) cells and supplied as a 0.2 um filtered solution in PBS (pH 7.4).
  5. "SARS-CoV-2 S2" also derived from HEK293 cells were used in experiments where indicated

Beyond the use of recombinant spikes cultured and grown in bacteria and human kidneys cells, the systems used to study the blood-brain barrier (BBB) were 2D and 3D models (i.e. recreations). The brain cells were cultured in rat tail collagen coated flasks along with medium containing fetal calf serum. Three-dimensional models of the blood-brain barrier (3D BBB) were fabricated by polymerizing hydrogels. The models are considered the best recapitulations (closest resemblance) to the real BBB. In other words, we have fake spike proteins being examined in fake 2D and 3D models representing the blood-brain barrier. There is nothing real about the material used nor the experiments performed and thus no conclusions about what occurs inside a living organism can be gained from this paper, especially regarding the idea that a spike protein can cause the loss of blood-brain barrier integrity and can trigger an inflammatory response in brain endothelial cells:

The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood–brain barrier

"To test functional outcomes, two (a 2D and a 3D vessel-like) in-vitro models of the BBB using primary brain endothelial cells were used. In both models, the effects of the spike subunits of SARS-CoV-2 on barrier integrity were determined. Our results provide evidence of endothelial barrier permeability and pro-inflammatory responses upon exposure to these subunits. Moreover, our analysis points to barrier breach that may be independent of ACE2 since deleterious effects also occurred with the S2 subunit. To the authors knowledge, this is the first evaluation for the effects of SARS-CoV-2 spike protein on the BBB."

2. Materials and methods

2.1. Reagents

"SARS-CoV-2 subunit S1 (RayBiotech, Cat No 230–01101), SARS-CoV-2 RBD (RayBiotech, Cat No 230–01102), and SARS-CoV-2 subunit S2 (RayBiotech, Cat No 230–01103) derived from E.coli and SARS-CoV-2 S1 (RayBiotech, Cat No 230–30161-10), SARS-CoV-2 S2 derived from HEK293 cells were used in experiments where indicated. We used SARS-CoV-2 spike protein subunits concentrations ranging from 0.1 nM to 50 nM based on a previous study that tested the effects of SARS-CoV-2 protein on stimulating human immune cells(Dosch et al., 2009). Other recombinant proteins (i.e TNFα) were purchased from R&D Systems (Minneapolis, MN, USA). Note, recombinant proteins diluted to the concentrations used for these studies were assayed for the presence of E.coli endotoxin using the ToxinSensor Chromogenic LAL Endotoxin Assay (GenScript) which found E.coli endotoxin levels to be only at negligible amounts.

2.2. Endothelial cell culture

Primary human brain microvascular endothelial cells (hBMVECs) were isolated from fetal brain tissue as described (Andrews et al., 2018). Healthy tissue was provided (under informed consent) by the Laboratory of Developmental Biology (University of Washington, Seattle, WA) with approval granted by Temple University's (Philadelphia, PA) Institutional Review Board and in full compliance by the National Institutes of Health's (NIH) ethical guidelines. Cells were grown on rat tail collagen I coated flasks (BD Biosciences) in full growth medium (EBM-2 medium supplemented with EGM-2MV SingleQuots (Lonza, Cat No CC-3156 and CC-4147)) in an incubator set to 37 °C, 5% CO2, and 100% humidity. Experiments were performed in the basal medium (EBM2 supplemented with 10% FBS).

For certain studies (as indicated in the figures), the hCMEC/D3 (a gift from Dr. Pierre O Couraud, Institut Cochin, université Paris Descartes, Paris, France) cell line that are often used for modeling the BBB were used. The cell line is a telomerase-immortalized human brain endothelial cell line for which its barrier forming properties and cell culture conditions have been previously characterized (Weksler et al., 2005).

2.3. 3D BBB model

Three-dimensional models of the blood-brain barrier (3D BBB) were fabricated by polymerizing hydrogels composed of 5 mg/mL type I collagen, 1 mg/mL hyaluronan, and 1 mg/mL Matrigel within microfabricated devices. The full method for this approach is described in a previous study (Partyka et al., 2017). Briefly, hydrogels were injected into the reservoir of the device and 180-μm needles coated in 0.1% BSA were inserted prior to polymerization to create two parallel and cylindrical voids within the gel. hCMEC/D3 were injected into one channel at a density of 10 million per mL (15 μL per channel). Channels were incubated for 10 min to ensure cell attachment then injected with cells again and inverted for 10 min to coat the opposing side to ensure full coverage. Following cell seeding, channels were exposed to 0.7 dyn/cm2 of steady shear stress for four days using a linear syringe pump (Kent Scientific) to establish barrier function. Following the four-day perfusion, vessels were perfused for two hours with 50 nM of SARS-CoV-2 subunit S1. Following exposure to the viral protein, vessels were either placed in fixative or prepared for permeability testing. To quantify localization of ZO-1 to the cell-cell junction in these vessels, the fluorescence intensities along representative 100-μm sections of both the control and spike protein-treated condition were plotted as described in a previous study (DeOre et al., 2019). The variance of both these intensity plots were calculated, and the percent difference was calculated to quantify the reduction in localization of ZO-1 to the cell-cell junctions."

"These systems (when also coupled with other cells) represent the most advanced recapitulation of the blood-brain barrier. Once the SARS-CoV-2 subunit S1 was introduced, the presence of barrier permeability (from lumen to parenchymal compartment) was clearly evident as early as 2 h. These results suggest that whether free viral spike proteins or those on the surface of the virus present during SARS-CoV-2 infection could induce barrier permeability (albeit once a certain threshold is reached) equivocal to the concentrations used here. As this is the first report on the topic, much work remains, particularly in regard to how permeability dynamics may change once these 3D microfluidic constructs are used with the whole SARS-CoV-2 virus."

https://www.sciencedirect.com/science/article/pii/S096999612030406X?via%3Dihub

"A study in Vaccines in January 2021 noted that the pathogenicity of the spike protein is a relevant concern for COVID‑19 vaccines since the mRNA vaccines are designed to instruct human cells to produce the spike protein of the coronavirus."

Hammond used this second study to claim that there is a concern that the spike protein, said to be created by the mRNA injection, can be pathogenic. What he didn't tell his readers is that this study once again used recombinant spike proteins created from cell cultures to "infect" cultured primary human pulmonary artery smooth muscle cells (SMCs) or cultured human pulmonary artery endothelial cells. As in the previous study, there is nothing natural about the experimental set up and design. The theoretical spike proteins we are said to encounter are not lab-created concoctions nor do these invisible entities interact with human tissues that have been potentially subjected to fetal bovine serum and other additives (the exact ingredients were not disclosed in the paper). Thus, any experimental results can only relate to the lab-created materials and conditions and can not be extrapolated to what happens under natural conditions within a living organism.

However, due to the results from the culture experiments along with what they claim is recent suggestive evidence, the researchers stated that it was reasonable to assume that the lab-created concoction said to harbor the spike protein can act alone in order to be pathogenic. Even though they did not test this, the researchers felt it was important to consider the possibility that the "SARS-CoV-2" spike protein produced by the new "COVID-19" vaccines (in an unobservable process) triggers cell signaling events that promote PAH, other cardiovascular complications, and/or complications in other tissues/organs in certain individuals. In other words, they were speculating about how the fictional spike protein may affect a living organism based on results from fake cultured spike proteins further cultured with human tissues in a petri dish in a lab:

SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Host Cells: Implications for Possible Consequences of COVID-19 Vaccines

3. SARS-CoV-2 Spike Protein Elicits Cell Signaling in Human Cells

"It was found that the treatment of cultured primary human pulmonary artery smooth muscle cells (SMCs) or human pulmonary artery endothelial cells with the recombinant SARS-CoV-2 spike protein S1 subunit is sufficient to promote cell signaling without the rest of the viral components [21]. Furthermore, our analysis of the postmortem lung tissues of patients who died of COVID-19 has determined that these patients exhibited pulmonary vascular wall thickening, a hallmark of pulmonary arterial hypertension (PAH) [21]. Based on these results, we proposed that the SARS-CoV-2 spike protein (without the rest of the viral components) triggers cell signaling events that may promote pulmonary vascular remodeling and PAH as well as possibly other cardiovascular complications [21,22].

In our cell culture experiments, two recombinant SARS-CoV-2 spike proteins, both of which contain the RBD, were studied [21]. The full-length S1 subunit protein contains most of the S1 subunit (Val16–Gln690), while the RBD S1 subunit protein only contains the RBD region (Arg319–Phe541), as shown in Figure 1. Cultured primary human pulmonary artery SMCs and human pulmonary artery endothelial cells were treated with these proteins for 10 min. We found, using the phospho-specific MEK antibody, that the recombinant full-length S1 subunit of SARS-CoV-2 alone at a concentration as low as 130 pM activated MEK, the activator of extracellular signal-regulated kinase (ERK) and a well-known signal transduction mechanism for cell growth [23]. By contrast, such activation of cell signaling by the spike protein did not occur in rat pulmonary artery SMCs [21]."

6. Discussion

"It is generally thought that the sole function of viral membrane fusion proteins is to allow the viruses to bind to the host cells for the purpose of viral entry into the cells, so that the genetic materials can be released and the viral replication and amplification can take place. However, recent observations suggest that the SARS-CoV-2 spike protein can by itself trigger cell signaling that can lead to various biological processes. It is reasonable to assume that such events, in some cases, result in the pathogenesis of certain diseases.

Our laboratory only tested the effects of the SARS-CoV-2 spike protein in lung vascular cells and those implicated in the development of PAH. However, this protein may also affect the cells of systemic and coronary vasculatures, eliciting other cardiovascular diseases such as coronary artery disease, systemic hypertension, and stroke. In addition to cardiovascular cells, other cells that express ACE2 have the potential to be affected by the SARS-CoV-2 spike protein, which may cause adverse pathological events. Thus, it is important to consider the possibility that the SARS-CoV-2 spike protein produced by the new COVID-19 vaccines triggers cell signaling events that promote PAH, other cardiovascular complications, and/or complications in other tissues/organs in certain individuals (Figure 3). We will need to monitor carefully the long-term consequences of COVID-19 vaccines that introduce the spike protein into the human body. Furthermore, while human data on the possible long-term consequences of spike protein-based COVID-19 vaccines will not be available soon, it is imperative that appropriate experimental animal models are employed as soon as possible to ensure that the SARS-CoV-2 spike protein does not elicit any signs of the pathogenesis of PAH or any other chronic pathological conditions."

https://www.mdpi.com/2076-393X/9/1/36/htm

"A study in Circulation Research in March 2021 showed that the spike protein alone can damage vascular endothelial cells.

"This study was cited by The Epoch Times to support its claim that the spike protein by itself is harmful, which Health Feedback attempted to rebut by noting that the research was done in hamsters using an engineered pseudovirus, which is incapable of intracellular replication, and was not a study of the effects of the spike protein in humans following vaccination. The study was "never designed to look at the toxicity of the spike protein after vaccination", Health Feedback correctly notes.

Health Feedback also cites Dr. Peter Hotez, a vaccine developer with Baylor College of Medicine, correctly observing that the study "looks at cellular mechanisms of how viral spike protein works, not the immune response from a vaccine."

Hammond used his third study to seemingly try and say that the spike protein can act alone to damage the vascular system. However, he immediately shares the Health Feedback critique stating that the study uses a pseudovirus, a limitation that even the researchers noted in their own paper.

Pseudoviruses are exactly what they sound like: fake (fake) "viruses." These are said to be recombinant "viruses" (i.e. lab-created cultured concoctions from many sources) which mix and match genetic material from other "viruses" making them "less virulent." This is how pseudoviruses are described according to the study Construction and applications of SARS-CoV-2 pseudoviruses: a mini review:

"Pseudoviruses are a kind of recombinant virus with their core or backbone and surface proteins derived from different viruses9. Genes inside pseudoviruses are usually altered or modified to abolish native surface protein expression. An additional plasmid is then used to express alternative surface proteins, producing a pseudovirus that can infect susceptible host cells but can only replicate intracellularly for a single round10, 11. As viral surface proteins play pivotal roles in gaining entry into host cells, the conformational structures of pseudoviral surface proteins have high similarity to that of the native viral proteins; however, pseudoviruses have attenuated virulence compared with wild-type (WT) viruses, allowing them to be safely handled in biosafety level 2 laboratories."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8071765/figure/F1/?report=objectonly

The strategies to acquire SARS-CoV-2 pseudoviruses based on different packaging systems. (a) HEK 293T cells were transfected with a plasmid encoding lentiviral backbone and a plasmid expressing SARS-CoV-2 Spike. The transfected cells produced Spike-pseudotyped lentiviral particles and these viral particles can infect cells that express the ACE2 receptor. (b) HEK 293T cells were co-transfected with an Spike encoding-plasmid, an MLV Gag-Pol packaging construct and the MLV transfer vector encoding a luciferase reporter. The transfected cells produced Spike-pseudotyped MLV particles and these viral particles can infect cells that express the ACE2 receptor. (c) HEK 293T cells were transfected with SARS-CoV-2 Spike expression plasmid, after 24 h post-transfection, the cells were inoculated with VSV*∆G (Fluc) encoding firefly luciferase. After an incubation period of 1h at 37 ℃, the inoculum was removed and cells were washed with PBS before medium supplemented with anti VSV-G antibody was added in order to neutralize residual input virus. Spike-pseudotyped particles were harvested 20 h postinoculation and could infect cells that express the ACE2 receptor.

Sadly, the researchers of the paper Hammond cited do not share how their pseudovirus was created, but from the above source we can obtain an idea of what was done through the cell culture process. The reseachers also claim that their findings using the fake (fake) "virus" need to be confirmed using the real (fake) "SARS-COV-2 virus." Thus, once again, we can see that the study cited does not reflect reality in any way. Any and all conclusions about how the spike protein of "SARS-COV-2" would affect the vascular system can not be gained from this paper. All that can be taken away is that when mixing and matching different cultures, different indirect chemical results are generated outside of any living organism in a lab which can then be interpreted by the researchers into a story of how a fictional entity they never studied may act or behave while within the human body. Then the headlines and snippets from the conclusions can be used by bloggers and "fact-checkers" to bolster a fraudulent case claiming that part of the fictional entity is pathogenic by itself:

SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2

"We administered a pseudovirus expressing S protein (Pseu-Spike) to Syrian hamsters intratracheally. Lung damage was apparent in animals receiving Pseu-Spike, revealed by thickening of the alveolar septa and increased infiltration of mononuclear cells (Figure [A])."

"Although the use of a noninfectious pseudovirus is a limitation to this study, our data reveals that S protein alone can damage endothelium, manifested by impaired mitochondrial function and eNOS activity but increased glycolysis. It appears that S protein in ECs increases redox stress which may lead to AMPK deactivation, MDM2 upregulation, and ultimately ACE2 destabilization.4 Although these findings need to be confirmed with the SARS-CoV-2 virus in the future study, it seems paradoxical that ACE2 reduction by S protein would decrease the virus infectivity, thereby protecting endothelium. However, a dysregulated renin-angiotensin system due to ACE2 reduction may exacerbate endothelial dysfunction, leading to endotheliitis. Collectively, our results suggest that the S protein-exerted EC damage overrides the decreased virus infectivity. This conclusion suggests that vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury."

https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.121.318902

"A study in The FASEB Journal in May 2021 found that the spike protein induces acute lung injury in mice genetically engineered to express the ACE2 receptor, which is the receptor on certain human cells that enables the coronavirus via the spike protein to fuse with and enter the cells where it then replicates."

Sadly, this next study remains blocked to me as I am unable to access the full paper. However, Hammond did supply a link which discussed the findings and from that article we can find out some interesting details:

"Studying SARS-CoV-2 can be challenging because experiments involving the intact virus requires a Biosafety Level 3 laboratory. To overcome this hurdle, the researchers created a new model of acute lung injury that utilizes transgenic mice that express the human receptor for SARS-CoV-2 in their lungs.

"Our mouse model dramatically reduces the danger of doing this type of research by allowing COVID-19 lung injury to be studied without using the intact, live virus," said Solopov. "This will greatly increase and diversify the ability to do COVID-19 research. Our model will also likely be useful for studying other coronaviruses."

The researchers injected the genetically modified mice with a segment of the spike protein and analyzed their response 72 hours later. Another group of mice received only saline to serve as a control.

The researchers found that the genetically modified mice injected with the spike protein exhibited COVID-19-like symptoms that included severe inflammation, an influx of white blood cells into their lungs and evidence of a cytokine storm – an immune response in which the body starts to attack its own cells and tissues rather than just fighting off the virus. The mice that only received saline remained normal."

What we can see is that transgenic mice were used in order to study the so-called spike protein. Transgenic mice are genetically-altered mice which are said to have been constructed by injecting cloned DNA into fertilized mouse eggs. The eggs that survive this process are then implanted into female mice in order to  develop them. These transgenic mice were then said to be injected with the spike protein into their throats. While I could not find any details about what spike protein was used in this study, it is reasonable to assume that this was yet another recombinant lab-created cultured protein as the researchers admitted to not using "live infectious virus" nor needing a level 3 biosafety laboratory.  The transgenic mice came down with "COVID-like" symptoms which consisted of severe inflammation, increased white blood cell counts in the lungs, and "evidence" of a cytokine storm (which was only mentioned in the article yet not in the abstract nor conclusion of the study).

Thus, we have a study utlizing genetically-altered mice that experienced inflammation when injected unnaturally in the throat with lab-created cultured recombinant goo. From these results, the researchers confidentally proposed that a single exposure of K18-hACE2 mice to "SARS-CoV-2" Spike Protein S subunit S1 may represent a valid model of "COVID-19" that may be useful for the preclinical investigation of new potential countermeasures against "COVID-19" and other "coronaviral" infections. Hardly a ringing endorsement, which is not surprising given the experimental set-up, yet this did not stop Hammond from including it as part of his litany of "favorable" evidence:

Single intratracheal exposure to SARS-CoV-2 S1 spike protein induces acute lung injury in K18-hACE2 transgenic mice

"The SARS-CoV-2 pandemic has infected more than 85,900,000 people and provoked the death of more than 1.9 million worldwide. Therapeutic options remain limited, and vaccines may exhibit narrow efficacy, due to short supplies, delays in distribution and the emergence of new resistant strains. It is mandatory to study new therapeutic approaches that modulate the strong inflammatory response observed in the lung, prevent respiratory failure and improve outcomes. The study of SARS-CoV-2 pathogenicity in vivo is challenging due to the necessary biosafety laboratory regulations. Thus, we developed an acute lung injury model by intratracheally instilling the S1 subunit of SARS-CoV-2 Spike S protein (400 µg/kg, 2 ml/kg body weight) in K18-hACE2 transgenic mice that overexpress the human receptor for SARS-CoV-2 Spike protein S, ACE2, and investigated outcomes 72 hours later. Mice exhibited an acute decline in body weight during the first 48 hours following instillation, compared to saline-instilled controls. At 72 hours, bronchoalveolar lavage fluid demonstrated a dramatic increase in white blood cell content, particularly neutrophils, and marked proteinosis compared to controls. Histologic examination of lung tissue revealed hyaline membranes, alveolar septal thickening, and a large number of neutrophils in the interstitial and alveolar spaces of Spike protein S exposed mice. We propose that a single exposure of K18-hACE2 mice to SARS-CoV-2 Spike Protein S subunit S1 may represent a valid model of COVID-19, allow the study of the molecular mechanisms of SARS-CoV-2 induced lung injury and be useful in the investigation of potential new therapeutic approaches to the management of COVID-19 as well as future coronavirus-dependent respiratory diseases.

Conclusions: We demonstrate for the first time that the intratracheal instillation of a single element of the SARS-CoV-2 virus, the subunit 1 of the Spike protein, in K18-hACE2 transgenic mice, is capable of eliciting strong pulmonary and systemic inflammation, including activation of the STAT3 and NFκB pathways in the lungs and biochemical and histological evidence of acute lung injury. We propose that this model may be useful for the preclinical investigation of new potential countermeasures against COVID-19 and other coronaviral infections."

The entirety of the "study?"

https://doi.org/10.1096/fasebj.2021.35.S1.04183

"A study in Clinical Infectious Diseases in May 2021 showed that the spike protein induced by Moderna's mRNA COVID‑19 vaccine circulates throughout the body."

The problem with Hammond's next study relates once again to the use of recombinant lab-created spike proteins as well as the use of serological results to conclude anything meaningful from the experimental procedures. This study attempts to claim that antibody results show that the spike protein, said to be created during the unobservable process after vaccination, circulates throughout the body. The researchers used different assays during the study and commented on the fact that no one had ever shown these kinds of results before. They admitted that this may have to do with the limitations of the assays themselves, thus showcasing the potential inaccuracy of their own results due to technological limitations.

Beyond the technological limitations is the problem of claiming that theoretical antibodies can detect theoretical spike proteins. In order for this to be true, the spike protein and the antibodies themselves must both be purified and isolated first and then experimented with together in order to show that they are specific to each other. As neither the spike protein nor the antibodies have ever been scientifically proven to exist in purified/isolated form, these results are essentially meaningless. One can not use one fictional entity to determine the presence and/or absence of another fictional entity. This is why non-specific results regularly occur with antibodies and we end up seeing statements from researchers such as "possibly due to assay cross-reactivity with other human coronaviruses" as we see in this study.

In any case, only 3 of 13 participants saw spike protein antibody results for 15 days after the first injection and none saw any spike protein antibody results for upwards of 56 days after the second injection. If the spike protein is supposed to circulate in the body after injection, based on these results, it doesn't appear to do so for very long if at all in the vast majority of the participants studied:

Circulating Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients

"Here we provide evidence that circulating SARS-CoV-2 proteins are present in the plasma of participants vaccinated with the mRNA-1273 vaccine. We report antigen and serological data of the mRNA-1273 vaccine in 13 healthcare workers at the Brigham and Women's Hospital. Ultrasensitive single-molecule array (Simoa) assays were used for the detection of SARS-CoV-2 antigens spike (S1–S2 unit), S1, and nucleocapsid and antibodies immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin M (IgM) against SARS-CoV-2 spike, S1, receptor binding domain (RBD), and nucleocapsid, as previously described [6, 7]."

"S1 antigen was detected as early as day 1 postvaccination, and peak levels were detected on average 5 days after the first injection (Figure 1A). The mean S1 peak level was 68 pg/mL ± 21 pg/mL. S1 in all participants declined and became undetectable by day 14. No antigen was detected at day zero for 12 of 13 participants, as expected. However, one individual presented detectable S1 on day zero, possibly due to assay cross-reactivity with other human coronaviruses or asymptomatic infection at the time of vaccination. Spike protein was detectable in 3 of 13 participants an average of 15 days after the first injection. The mean spike peak level was 62 pg/mL ± 13 pg/mL. After the second vaccine dose, no S1 or spike was detectable, and both antigens remained undetectable through day 56. For one individual (participant 8), spike was detected at day 29, 1 day after the second injection and was undetectable 2 days later."

"We observe an increase in S1 over an initial period of 1–5 days, suggesting that mRNA translation begins immediately after vaccine inoculation. Interestingly, spike protein appears in 3 of 13 participants on average 8 days after S1 is produced. The Simoa antigen assays for the full spike protein are designed to require antibody binding to both the S1 and S2 subunits for detection, resulting in a cleaved spike protein to be undetectable. Additionally, spike protein concentrations in plasma of vaccinated participants may be below our assay limit of detection. We hypothesize that the cellular immune responses triggered by T-cell activation, which would occur days after the vaccination, lead to direct killing of cells presenting spike protein, and an additional release of spike into the blood stream [9]. The mechanisms underlying release of free S1 and the subsequent detection of the intact spike protein remain unclear and require further studies."

"Limitations of the current study include the small sample size and potential biases that result from enrolling healthy, young adults, which may not be representative of the general population. Future studies should also examine the dynamics of antigen production with neutralization antibodies. Nonetheless, evidence of systemic detection of spike and S1 protein production from the mRNA-1273 vaccine is significant and has not yet been described in any vaccine study, likely due to limitations in assay sensitivity and timing assessment. The clinical relevance of this finding is unknown and should be further explored."

From the supplemental material:

"SARS-CoV-2 Spike protein (produced in Bing Chen's lab), Nucleocapsid recombinant protein (Ray Biotech 230-30164), S1 protein (Sino Biological 40591-V08H), and RBD (produced in Aaron Schmidt's lab) were conjugated to 647 nm, 488 nm, 700 nm, and 750 nm dye-encoded carboxylated paramagnetic beads (Quanterix), respectively, using EDC (1-ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride) chemistry (ThermoFisher Scientific 77149)."

https://academic.oup.com/cid/article/74/4/715/6279075?login=false

"The authors of a paper published on the preprint website Authorea in May 2021 expressed concern that government authorities were minimizing or ignoring concerns about the potential toxicity and pathogenicity of the spike protein induced by vaccination. (A preprint study is one that has not yet undergone peer review.)"

This next paper is more of a commentary than an actual study. While the authors are right to suggest that the adverse vaccine reactions that occur can and will be counted as cases of "SARS-COV-2," the evidence used to claim that the spike protein is pathogenic and the potential cause is based on Hammond's earlier fraudulent study which used pseudoviruses and hamsters. Again, I am not stating that the vaccines are not dangerous. They most definitely are dangerous and toxic. However, the story that there is a pathogenic spike protein created from the mRNA injection is nothing but pure science fiction based upon fraudulent evidence that is circulated by those aiming to keep the confused public believing in the germ theory lie. Ironically, the authors end their commentary by saying that "relying on a careful evaluation of the relevant scientific research, is urgent" and that it "is imperative to follow the science." Sadly, it appears that they did no such thing:

SARS-CoV-2 mass vaccination: Urgent questions on vaccine safety that demand answers from international health agencies, regulatory authorities, governments and vaccine developers   

"Furthermore, even in the absence of SARS-CoV-2 virus, Spike glycoprotein alone causes endothelial damage and hypertension in vitro and in vivo in Syrian hamsters by down-regulating angiotensin-converting enzyme 2 (ACE2) and impairing mitochondrial function [26]. Although these findings need to be confirmed in humans, the implications of this finding are staggering, as all vaccines authorized for emergency use are based on the delivery or induction of Spike glycoprotein synthesis. In the case of mRNA vaccines and adenovirus-vectorized vaccines, not a single study has examined the duration of Spike production in humans following vaccination. Under the cautionary principle, it is parsimonious to consider vaccine-induced Spike synthesis could cause clinical signs of severe COVID-19, and erroneously be counted as new cases of SARS-CoV-2 infections. If so, the true adverse effects of the current global vaccination strategy may never be recognized unless studies specifically examine this question. There is already non-causal evidence of temporary or sustained increases in COVID-19 deaths following vaccination in some countries (Fig. 1) and in light of Spike's pathogenicity, these deaths must be studied in depth to determine whether they are related to vaccination."

"An open scientific dialogue is urgent and indispensable to avoid erosion of public confidence in science and public health and to ensure that the WHO and national health authorities protect the interests of humanity during the current pandemic. Returning public health policy to evidence-based medicine, relying on a careful evaluation of the relevant scientific research, is urgent. It is imperative to follow the science."

https://www.authorea.com/users/414448/articles/522499-sars-cov-2-mass-vaccination-urgent-questions-on-vaccine-safety-that-demand-answers-from-international-health-agencies-regulatory-authorities-governments-and-vaccine-developers?commit=123b84611353b243b6d09320ac98cb07db022771

"Ironically, Dr. Peter Hotez, whom Health Feedback cites to support its argument that the spike protein induced by vaccination is harmless, was among the authors of a study published in the journal Circulation in July 2021 noting that mRNA COVID‑19 vaccines can cause myocarditis, or inflammation of the heart, and hypothesizing that this might be due to some individuals' immune response to either vaccine mRNA or the vaccine-induced spike protein."

Hammond next supplied a review article by Dr. Peter Hotez which he used as evidence that the mRNA vaccine can cause myocarditis. In the review, Dr. Hotez and the other authors hypothesized (an educated guess) that myocarditis could be due to the spike protein. However, in the paper it was admitted that the mechanisms for the development of myocarditis were unknown and several possible proposals were listed. The study that was cited in the review which was used as evidence for the hypothesized role that the spike protein plays in myocarditis, used recombinant spike protein and commercially available antibodies in order to obtain the results. Once again, we have hypothetical conclusions crafted around results from lab-created concoctions which have no bearing on reality:

"Although the mechanisms for development of myocarditis are not clear, molecular mimicry between the spike protein of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and self-antigens, trigger of preexisting dysregulated immune pathways in certain individuals, immune response to mRNA, and activation of immunologic pathways, and dysregulated cytokine expression have been proposed."

"Another important potential mechanism for myocarditis is molecular mimicry between the spike protein of SARS-CoV-2 and self-antigens.50 Antibodies against SARS-CoV-2 spike glycoproteins have been experimentally shown to cross-react with structurally similar human peptide protein sequences, including α-myosin.50 However, severe adverse events or autoimmune reactions have been very rare.46,47 Although COVID-19 vaccination does not appear to provoke de novo immune-mediated adverse events, it is possible that it may trigger preexisting dysregulated pathways in certain individuals with predisposition, resulting in a polyclonal B-cell expansion, immune complex formation, and inflammation.48″

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.121.056135

Link 50 takes us to this study:

Potential antigenic cross-reactivity between SARS-CoV-2 and human tissue with a possible link to an increase in autoimmune diseases

"Commercially available mouse monoclonal antibody made against recombinant SARS coronavirus spike protein and rabbit monoclonal antibody made against SARS coronavirus nucleoprotein were applied at optimal dilution to the SARS-CoV-2 proteins and to 50 different tissue antigens using enzyme-linked immunosorbent assay (ELISA). Recombinant SARS-CoV-2 spike protein S1 and recombinant SARS-CoV-2 nucleocapsid protein were purchased from RayBiotech. ELISA wells were coated with nuclear antigens, dsDNA, F-actin, and mitochondria (M2) antigen purchased from different companies. An additional 45 tissue antigens used in this study have been previously described [9]."

https://www.sciencedirect.com/science/article/pii/S1521661620304253?via%3Dihub

"A study published at the preprint server bioRxiv in July 2021 found an association between "Long Covid" and persistence of the spike protein in the absence of persistence of whole viable virus, once again indicating that the spike protein alone is pathogenic."

This next study provided by Hammond tried to make the case that detecting the spike protein RNA without finding whole "SARS-COV-2" RNA/genome was sufficient to claim that the spike protein itself was pathogenic and persisting within the body. To deternine this, the researchers first used digital droplet PCR to find "SARS-COV-2" RNA in the blood of a few patients, thus relying on a fraudulent test and genome to determine the initial findings. This step resulted in 36% (4 of 11) of severe "COVID-19" patients' PBMCs contained "SARS-CoV-2" RNA compared to 4% (1/26) of PASC patients' PBMCs. The researchers then decided to use flow cytometry with antibodies said to define B cell, T-cell, and monocytic subsets in addition to simultaneous staining of these cells with an antibody claimed to be specific to the "SARS-CoV-2" S1 protein to try and determine the reservoir for the detected RNA. To confirm the presence of "SARS-CoV-2" S1 protein, they then sorted CD14lo, CD16+ monocytes and performed Ultra High-Performance Liquid Chromatography. After various preparation processes, the researchers measured the peptides coming from peripheral blood monolayers (stored in 90% fetal bovine serum) and compared them to a peptide database from a commercially made recombinant spike protein and found up to 44% (i.e. up to = not always that high) of the S1 subunit peptides could be identified in patient samples. In other words, the researchers used indirect measurements of peptides matched between patient samples and recombinant spike proteins which were mapped to a peptide database created from the commercially made recombinant protein in order to claim INDIRECTLY that the spike protein was in the patients samples. Can you spot the circular methods there?

Worse yet, full length sequencing of the five cases submitted for genomic analysis failed to identify any full-length sequence in the spike protein gene, or any other gene, that could account for the observed spike protein detected by proteomic analysis. All they could find were fragments of "SARS-COV-2" genomes. Thus, they concluded that it must not be replication competent "virus" that was found but non-infectious leftover spike proteins which were not cleared from the body. As can be seen, this smattering of indirect evidence is based upon a "virus" and spike protein that was never properly purified and isolated first in order to accurately determine any specific antibody responses nor determine an accurate genome and peptide database. Thus, all measurements used to indirectly claim the presence of the spike protein are based on results coming from fraudulent lab-generated cultured creations:

Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection

"Since the reports by our group and others found that monocyte subsets can be infected by HIV, HCV, Zika virus and Dengue fever virus (1012), we screened peripheral blood mononuclear cells (PBMCs) from PASC individuals, as well as acute severe COVID-19 as controls, for SARS-CoV-2 RNA (Table 1). Using the highly sensitive, quantitative digital droplet PCR (ddPCR), we found that 36% (4 of 11) of severe COVID-19 patients' PBMCs contained SARS-CoV-2 RNA compared to 4% (1/26) of PASC patients' PBMCs. The one PASC patient that was RNA positive was 15 months post infection.

To further establish the exact reservoir contributing to the positive signal detected using ddPCR, we performed high parameter flow cytometry with antibodies that define B cell, T-cell, and monocytic subsets in addition to simultaneous staining of these cells with an antibody for the SARS-CoV-2 S1 protein. As demonstrated in Figure 2, we found distinct subpopulations of SARS-CoV-2 containing cells in the CD14lo, CD16+ monocytic subset for 73% (19 out of 26) of PASC patients and 91% (10 out of 11) of severe COVID-19 patients. As demonstrated in Figure 3, the quantity of SARS-CoV-2 S1 containing cells were statistically significant in both the severe patients (P=0.004) and in the PASC patients (P=0.02). Neither classical monocytes nor intermediate monocytes expressed the SARS-CoV-2 S1 protein.

To confirm the presence of SARS-CoV-2 S1 protein, we sorted CD14lo, CD16+ monocytes and performed Ultra High-Performance Liquid Chromatography (UHPLC). Following immunoprecipitation, the elution fractions were dried down in vacuo, resuspended in ddH2O and purified by to remove any non-crosslinked SARS-CoV-2 S1 antibody as well as any detergents from the commercial immunoprecipitation buffers. The UHPLC collected fractions were dried in vacuo, resuspended in 100 mM HEPES (pH 8.0, 20% Acetonitrile), and subjected to cistern: reduction and alkylation with chloroacetamide. The samples were then digested with AspN and LysC endopeptidases for 16h at 37°C. The digested peptides were analyzed on an Agilent 6550 IonFunnel QTOF and 1290 UHPLC by comparing patient samples to identical digests performed on commercially available SARS-CoV-2 S1 subunit. S1 subunit peptides from patient samples were mapped to a peptide database generated using commercial S1 subunit digests. Peptide identification consisted of matches in exact mass, isotope distribution, peptide charge state, and UHPLC retention time. As shown in Figure 4, the retention time of the representative peptide NLREFVFK in the digested commercial S1 subunit and Sample LH1-6 matched. Additionally, the Mass Spectra in Figure 4 show identical mass, isotope distribution, and charge states for the representative peptide NLREFVFK in the representative LH1 sample and commercial S1 subunit (also observed in LH 2-6, not shown). Using these metrics, up to 44% of the S1 subunit peptides could be identified in patient samples LH1-LH6 (Supplementary Table 1), providing complementary evidence to flow cytometry experiments that demonstrate the presence of S1 subunit protein in these patient cells."

"Cells from 4 out of 11 severe COVID-19 patients and 1 out of 26 PASC patients contained ddPCR+ peripheral blood mononuclear cells, however, only fragmented SARS-CoV-2 RNA was found in PASC patients. No full length sequences were identified, and no sequences that could account for the observed S1 protein were identified in any patient."

"It is important to note that the S1 protein detected in these patients appears to be retained from prior infection or phagocytosis of infected cells undergoing apoptosis and is not the result of persistent viral replication. Full length sequencing of the five cases submitted for genomic analysis failed to identify any full-length sequence in the spike protein gene, or any other gene, that could account for the observed spike protein detected by proteomic analysis."

High Parameter Immune Profiling/Flow Cytometry

Peripheral blood mononuclear cells were isolated from peripheral blood using Lymphoprep density gradient (STEMCELL Technologies, Vancouver, Canada). Aliquots 200 of cells were frozen in media that contained 90% fetal bovine serum (HyClone, Logan, UT) and 10% dimethyl sulfoxide (Sigma-Aldrich, St. Louis, MO) and stored at -70°C. Cells were stained and analyzed using a 17-color antibody cocktail including a PE-labeled SARS-CoV-2 S1 antibody (BioTechne, Minneapolis MN).

LC-MS analysis

Digested recombinant SARS-CoV-2 Spike S1 protein was analyzed by a high mass accuracy mass spectrometer to generate a list of detectable peptides with retention time and accurate masses. An Agilent 1290 Infinity II high pressure liquid chromatography (HPLC) system and an AdvanceBio Peptide Mapping column (2.1 × 150 mm, 2.7 μm) were used for peptide separation prior to mass analysis."

https://www.biorxiv.org/content/10.1101/2021.06.25.449905v3.article-info

"A study in Viruses in October 2021 found that the spike protein can enter the nucleus of cells and inhibit DNA damage repair. The authors noted that this finding was relevant for mRNA COVID‑19 vaccines since they are designed to elicit human cells to produce the spike protein."

Interestingly, this next source supplied by Hammond to state that the spike protein can enter the nucleus of cells and inhibit DNA damage repair was actually retracted May 10th, 2022, well over a month before his article was published on June 28th, 2022.

Retraction published on 10 May 2022, see Viruses 202214(5), 1011.

This is a perfect example as to why one should never just read the headline and throw any study out there in support of an argument without actuallly having read the study first. All claims from this paper which were used by Hammond in support of his spike protein argument are therefore false and invalid:

SARS–CoV–2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In Vitro

"The published article [1] has been retracted. Following publication, the first author contacted the editorial office regarding an improper experimental design with the potential to significantly affect the integrity of the resultant experimental data.

Adhering to our complaint procedure, an investigation was conducted. Both the chosen construct of the spike plasmid that contained a C-terminal fused with 6xHis tag and use of a GFP reporter system under overexpression conditions in the protocol were identified as having the potential to introduce significant ambiguity regarding the nature of the reported observations. The reliability of the results and conclusions presented have therefore been undermined. Furthermore, statements regarding the effect of the spike protein on the adaptive immunity are misleading as in this article no experiments related to the adaptive immunity were performed, and the full-length spike-based vaccine was not studied. Therefore, conclusions related to vaccine safety are not validated and lacked experimental support. This article [1] is retracted and shall be marked accordingly. This retraction was approved by the Editor-in-Chief of the journal Viruses."

https://www.mdpi.com/1999-4915/13/10/2056/htm

"A study in the Journal of Immunology in November 2021 found that the spike proteins induced by the Pfizer-BioNTech COVID‑19 vaccine are carried by extracellular vesicles called exosomes and circulate throughout the body, which helps to explain the blood antibody response elicited by vaccination."

In Hammond's next study, it is claimed that the vaccines create exosomes which carry spike proteins on their surface that circulate throughout the body. This is yet another serological study attempting to claim that the antibodies used are specific to a spike protein which was used in order to stain the exosome so that the spike proteins can be visualized. However, once again it must be stated that in order to deternine specific antibody responses, the "virus," it's spike protein, the antibody, and the exosomes would have needed to have been properly purified and isolated directly from the fluids of humans first. This has never been done and thus these all remain unproven fictitious entities which can not be used in order to verify the existence of the other. This is yet another study using recombinant cultured goo said to contain spike proteins and not purified/isolated particles proven to be spike proteins. It all amounts to nothing more than staining fluids and pointing and declaring at the dots which stick to a blob in EM and claiming this as proof that exosomes with spike proteins were created from vaccination:

Cutting Edge: Circulating Exosomes with COVID Spike Protein Are Induced by BNT162b2 (Pfizer–BioNTech) Vaccination prior to Development of Antibodies: A Novel Mechanism for Immune Activation by mRNA Vaccines

"In the current study, we analyzed eight healthy adults who received both doses of the SARS-CoV-2 vaccine (Pfizer–BioNTech). Our results demonstrated the induction of circulating exosomes carrying the SARS-CoV-2 spike protein by day 14, when Abs to the spike protein were not detectable in the sera using an ELISA method developed in our laboratory. Circulating Abs were detectable only after the second booster dose of vaccine (days 14), and the amount of exosomes containing spike protein was increased up to ∼12-fold maximum."

Materials and Methods Patient cohort and demographics

We analyzed eight healthy adult volunteers vaccinated with the mRNA-based SARS-CoV-2 vaccine (Pfizer–BioNTech). Blood was collected before vaccination, days 7 and 14 after the first dose, day 14 after the second dose, and 4 mo after both the doses. This study was approved by the Institutional Review Boards (IRB) at St. Joseph's Hospital (IRB number PHXB16-0027-10-18).

Exosome isolation and nanoparticle tracking analysis

Exosomes were isolated from 500 µl of plasma using Invitrogen Exosome Isolation Kit followed by 0.22-micron filtration (7). All exosomes were analyzed for size by NanoSight NS300 (Malvern Panalytical, Great Malvern, U.K.), and the mean size of the particles used in our experiments was <200 nm (8).

Detection of Abs to SARS-CoV-2 spike protein and nucleocapsid protein from human plasma samples

Development of Abs to SARS-CoV-2 spike Ag was determined using an ELISA developed in our laboratory. In brief, 1 μg/ml SARS-CoV-2 spike protein (Sino Biological) suspended in PBS was coated on an ELISA plate and incubated overnight at 4°C. Human plasma was added to these plates at 1:750 dilution. Detection was performed using secondary anti-human IgG-HRP (1:10,000) and developed using tetramethylbenzidine substrate and read at 450 nm."

Transmission electron microscopy of isolated exosomes for SARS-CoV-2 spike protein

"Exosomes were labeled with immunogold and mouse anti–SARS-CoV-2 spike Ab, and coronavirus FIPV3-70 Ab (1:100) was added to the grids. Grids were washed and stained with uranyl acetate and viewed by transmission electron microscopy (JEOL USA, Peabody, MA) (10)."

"We performed transmission electron microscopy using Abs specific for SARS-CoV-2 spike to demonstrate the presence of SARS-CoV-2 Ags on the surface of exosomes from controls and healthy vaccinated individuals. Exosomes from vaccinated individuals are positive for SARS-CoV-2 Ag (Fig. 1B). We have also stained both the exosome samples with coronavirus FIPV3-70 Ab as negative control and did not observe any positive reaction in exosomes (Fig. 1B)."

See the tiny black dots? Those are the "spikes."

https://www.jimmunol.org/content/207/10/2405#ref-7

"A study in Clinical Science in December 2021 tested the hypothesis that the spike protein "may act as a ligand to induce non-infective cellular stress". They showed that exposure to the spike protein alone "elicited signalling and functional alterations", including "secretion of pro-inflammatory molecules typically involved in the cytokine storm" and "production of pro-apoptotic factors" causing endothelial cell death.

Health Feedback briefly notes this study by saying that it "showed that the spike protein can affect heart cells in the lab, but they used higher amounts of the protein than those found in COVID‑19 patients."

Nevertheless, the study did demonstrate a biologically plausible mechanism by which blood clots could occur with SARS‑CoV‑2 infection or vaccination."

This was another study used by Hammond to try and claim that the spike protein alone is pathogenic. He believed that the study showed a plausible way blood clots may occur due to "SARS-COV-2" and/or injection from the mRNA vaccine. However, once again, this study did not use purified and isolated particles but instead experimented with lab-created recombinant S proteins made from insect cells. The primary cell cultures used for the study were grown in dedicated medium supplemented with human recombinant growth factors and 2% fetal calf serum which hardly sounds like something the cells would encounter within a living organism. These cells were passaged between 4 to 7 times which can have detrimental effects on the culture as the passage number increases. The cell line cultures consisted of human gut epithelial cell line, Caco2, expressing hACE2 as well as African green monkey kidney cell line VeroE6 engineered to overexpress the human ACE2 and TMPRSS2. All cells were cultured in Dulbecco's modified Eagle's medium plus GlutaMAX supplemented with 10% FBS, 1% sodium pyruvate, and 0.1 mM non-essential amino acids. The human lung epithelial cell line Calu3 (ATCC HTB-55) was cultured in Eagle's minimum essential medium plus GlutaMAX with 10% FBS, 0.1 mM non-essential amino acids, and 1% sodium pyruvate. In other words, there is absolutely nothing natural about the materials nor the chemical additives that they were kept in and experimented with.

The researchers stated that their study provided novel (as in fictional) proof-of-concept evidence for S protein capacity to cause molecular and functional changes in human vascular PCs. However, they admitted that their small sample size was inadequate and that further investigation in a larger population of patients was warranted to determine the cause for the inter-individual variability in PC infection. They also could not exclude that different scenarios may happen in vivo, i.e. within a living organism, as compared to that seen in vitro, i.e. inside a petri dish in a lab, thus essentially admitting that their results can not be applied to what occurs within a human body. Interestingly, the researchers also admitted that low amounts of the S protein could be detected in pre-pandemic control sera. They stated that this could be explained by the sequence homology between some regions of the S protein and other human proteins/peptides. In other words, the S protein contains similar sequences to normal human proteins/peptides and thus the tests that the researchers were using may have been picking up nothing more than normal human proteins/peptides rather than the theoretical S protein. Sadly, the immunogen sequence for the ELISA kit they used was locked away behind proprietary information (as is always the case), and therefore they could not determine if it recognised the S protein residues that have homology with unrelated peptides. Thus, the results from this study truly were worthless:

The SARS-CoV-2 Spike protein disrupts human cardiac pericytes function through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease 

"Exposure to the recombinant S protein alone elicited signalling and functional alterations, including: (1) increased migration, (2) reduced ability to support endothelial cell (EC) network formation on Matrigel, (3) secretion of pro-inflammatory molecules typically involved in the cytokine storm, and (4) production of pro-apoptotic factors causing EC death."

Primary cell cultures

"Cardiac PCs were immunosorted as CD31neg/CD34pos cells from human myocardial samples, and expanded in a dedicated medium supplemented with human recombinant growth factors and 2% v/v foetal calf serum (FCS) (ECGM2 complete kit, C-22111, PromoCell) as previously described [11,28]. Briefly, samples were finely minced using scissors and scalpel until nearly homogenous and digested with Liberase (Roche) for up to 1 h at 37 C, with gentle rotation. The digest was passed through 70-, 40-, and 30-μm strainers. Finally, the cells were recovered and sorted using anti-CD31 and -CD34 microbeads (Miltenyi) to deplete the population of CD31pos ECs and select CD31neg/CD34pos cells, which distinguish a population of perivascular cells in situ [11,28]. After expansion to passage 3, the purity of the cell population was verified using immunocytochemistry (ICC) or flow cytometry [11,28].

Human coronary artery ECs (CAECs) were purchased from PromoCell and expanded in the same medium used for PCs. All cells used in the present study tested negative for mycoplasma contamination (assessed using the PCR Mycoplasma Test Kit I/C, PromoCell, cat# PK-CA91-1096). Cells were used between passages 4 and 7.

Cell line cultures

The human gut epithelial cell line, Caco2, expressing hACE2 (Caco-2-ACE2) was a kind gift from Dr Yohei Yamauchi, University of Bristol. The African green monkey kidney cell line VeroE6 engineered to overexpress the human ACE2 and TMPRSS2 (VeroE6/ACE2/TMPRSS2) [29] was a kind gift from Dr Suzannah Rihn, MRC-University of Glasgow Centre for Virus Research. All cells were cultured in Dulbecco's modified Eagle's medium plus GlutaMAX (DMEM, Gibco, Thermo Fisher, cat# 10567014) supplemented with 10% v/v FBS (Gibco, Thermo Fisher, A3840001), 1% v/v sodium pyruvate, and 0.1 mM non-essential amino acids. The human lung epithelial cell line Calu3 (ATCC HTB-55) was cultured in Eagle's minimum essential medium plus GlutaMAX (MEM, Gibco, Thermo Fisher, cat# 41090036) with 10% v/v FBS, 0.1 mM non-essential amino acids, and 1% v/v sodium pyruvate."

Measurement of S protein in patients' sera

"The presence of S protein in COVID-19 patients' serum was evaluated using the COVID-19 Spike Protein ELISA Kit from Abcam (ab274342), according to manufacturer's instructions. Pre-pandemic sera were employed as controls. All test sera were diluted 1:2. The S protein concentration was expressed as nanogram per millilitre serum. The antibody supplied in the kit recognised the S2 domain."

Production and purification of the recombinant SARS-CoV-2 S protein

"SARS-CoV-2 S protein was expressed in insect cells and purified as described previously [33,35]. Briefly, the S construct encoded amino acids 1–1213 (extracellular domain – ECD) fused with a thrombin cleavage site, followed by a T4-foldon trimerisation domain and a hexahistidine (HIS) affinity purification tag at the C-terminus. The polybasic furin cleavage site was mutated (RRAR to A) to increase the stability of the protein for in vitro studies [33,35]. S protein was expressed in Hi5 cells using the MultiBac system [36]. Secreted S protein was harvested 3 days after infection by centrifuging the cell culture at 1000×g for 10 min followed by another centrifugation of supernatant at 5000×g for 30 min. S protein-containing medium was incubated with HisPur Ni-NTA Superflow Agarose (Thermo Fisher Scientific) for 1 h at 4°C. Resin bound with S protein was separated from unbound proteins and medium using a gravity flow column, followed by 30 column volume wash with wash buffer (65 mM NaH2PO4, 300 mM NaCl, 20 mM imidazole, pH 7.5). Finally, the protein was eluted with a step-gradient of elution buffer (65 mM NaH2PO4, 300 mM NaCl, 235 mM imidazole, pH 7.5). Eluted fractions were analysed by reducing SDS/PAGE. Fractions containing the S protein were pooled and concentrated using 50-kDa MWCO Amicon centrifugal filter units (EMD Millipore). During concentration, proteins were buffer-exchanged in PBS, pH 7.5. Concentrated protein was aliquoted, flash-frozen in liquid nitrogen, and stored at −80°C until use. In all the in vitro experiments of the manuscript, we will refer to the S-ECD protein simply as S protein.

Recombinant Spike S1 (#10522-CV) and S2 (#10584-CV) were purchased from R&D, resuspended in PBS according to manufacturer's instructions, aliquoted and stored at −80°C until use. Similarly to the S-ECD, the S1 and S2 proteins were produced in insect cells."

Discussion

"Our study provides novel proof-of-concept evidence for S protein capacity to cause molecular and functional changes in human vascular PCs, either dependently or independently of the CD147 receptor (summarised in Figure 11)."

"Here, we report that two-third of patients tested did not have their PCs infected by SARS-CoV-2, while the rate of infection was below 8% in the remaining subjects, suggesting a very low permissiveness of these cells to the coronavirus, at least in vitro."

"Further investigation in a larger population of patients is warranted to determine the cause for the inter-individual variability in PC infection. Moreover, we cannot exclude different scenarios may happen in vivo."

"In our study, low amounts of the S protein could be detected in pre-pandemic control sera. This could be explained by the sequence homology between some regions of the S protein and other human proteins/peptides. A previous report identified pathogenic regions of SARS-CoV-1 S protein, which share sequence homology with Angrgm-52 (GenBank accession number AAL62340), a novel gene up-regulated in human mesangial cells stimulated by angiotensin II and bradykinin [53]. Unfortunately, the immunogen sequence for this particular ELISA kit ab274342 is proprietary information, therefore we could not determine if it can recognise the S protein residues that have homology with unrelated peptides."

Study limitations

"The study was conducted on isolated cells and therefore the evidence must be confirmed in vivo.

The amount of S protein used for in vitro studies was higher than the average S protein concentration detected in COVID-19 patients' serum. However, circulating S protein represents the spill-over from infected organs, where concentration may be higher due to retention at the receptor level. Because we do not have access to post-mortem myocardial samples, we could not verify this hypothesis."

https://portlandpress.com/clinsci/article/135/24/2667/230273/The-SARS-CoV-2-Spike-protein-disrupts-human

"A study at bioRxiv on December 2021 showed that the SARS‑CoV‑2 spike protein by itself promoted platelet activation, which the authors suggested was "a pathogenic mechanism to explain thrombosis associated to COVID‑19 lung disease, by which Spike present in SARS‑CoV‑2 virions or exposed on the surface of infected cells, leads to platelet stimulation and subsequent activation of the coagulation cascade." (Emphasis added.)

That study was also cited by The Epoch Times, to which Health Feedback responded by noting that the researchers "studied the mechanisms for formation of blood clots, showing that spike protein can activate platelets in the lab but they did not establish if this happened at concentrations found in patients or vaccinated people."

In this second to last study, Hammond relied on a preprint non-peer-reviewed paper to share the author's suggestion that the spike protein can act alone in order to cause thrombosis in "Covid" patients. The paper comes with the below warning that the study should not be reported as conclusive:

A reminder: they have not been formally peer-reviewed and should not guide health-related behavior or be reported in the press as conclusive.

Interestingly, in a moment of shooting his own argument in the foot, Hammond pointed out that the Health Feedback article rightly stated that the results were only relevant in the lab and that the researchers did not establish if the results with the recombinant spike protein happened at concentrations found in patients or vaccinated people. This may have to do with the fact that, once again, the study relied on cell-cultured creations and "pseudoviruses" to generate their conclusions.

For some reason, I was unable to copy/paste the relevant sections from the study but I am providing the methods section from the abstract as well as a few images from the PDF showing that the researchers utilized cell cultured creations and lab-created "pseudoviruses" for their experiments. You can see the various processes used to create their fictional entity. Thus, once again, the experimental results do not reflect reality in any way:

SARS-CoV-2 Spike protein activates TMEM16F-mediated platelet pro-coagulant activity

"Methods We produced SARS-CoV-2 Spike or VSV-G protein-pseudotyped virions, or generated cells expressing Spike on their plasma membrane, and tested their effects on platelet adhesion (fluorescence), aggregation (absorbance), exposure of phosphatidylserine (flow cytometry for annexin V binding), calcium flux (flow cytometry for fluo-4 AM), and clot formation and retraction. These experiments were also conducted in the presence of the TMEM16F activity inhibitors Niclosamide and Clofazimine."

https://www.biorxiv.org/content/10.1101/2021.12.14.472668v2

"A commentary in Clinical Science on March 29 of this year summarized the state of knowledge about the pathogenicity of the spike protein alone:"

Finally, we have made it to the last of Hammond's exhausting list of pseudoscientific sources he seemingly failed to read. This one is a commentary on the state of "knowledge" on the lab-created recombinant and/or pseudovirus spike protein acting pathogenically alone. In other words, it added nothing new and actually used the same Avolio et al. study Hammond used which I outlined two sections above. If you can recall, this was the study which utilized lab-created recombinant S proteins made from insect cells for their experiments. The reseachers could not exclude that different scenarios may happen in vivo, i.e. within a living organism, as compared to that seen in vitro, i.e. inside a petri dish in a lab, thus essentially admitting that their results can not be applied to what occurs within a human body. They also admitted that the S protein contains similar sequences to normal human proteins/peptides and that the tests that the researchers were using may have been picking up nothing more than normal human proteins/peptides rather than the theoretical S protein. In other words, the evidence that the spike protein acts alone pathogenically from this commentary is as worthless as the Avolio et al. study from which it came:

"The concept that the S protein can cause detrimental effects in COVID-19 patients independent of infection could partially explain the long-term health issues."

"There has been extensive evaluation of SARS-CoV-2 infection and COVID-19 on cardiovascular health [1,2]; however, there is emerging evidence that the S protein shed from SARS-CoV-2 can circulate in the blood of patients and have detrimental consequences [3,10,11]. (Figure 1) The study by Avolio et al. in this issue of Clinical Science provides strong evidence that the circulating S protein could be more detrimental to cardiac health than infection of SARS-CoV-2 to the heart [3]. More specifically, the S protein was found to act through the CD147 receptor on human cardiac pericytes to cause microvascular dysfunction [3]. The authors also determined that the S protein caused human cardiac pericyte inflammation via yet to be determined mechanisms [3]."

"The current study by Avolio et al. found similar results with the Alpha and Delta variants of the S protein on human cardiac pericytes [3]. Although the findings of the current study are provocative, future investigations need to expand the doses of S proteins to lower levels and other S protein variants for in vitro studies. Lastly, as we investigate SARS-CoV-2 and the circulating S protein and the impact on human health, we will be better prepared to treat patients as COVID-19 moves from a pandemic to an endemic status."

https://portlandpress.com/clinsci/article/136/6/431/231092/SARS-CoV-2-spike-protein-causes-cardiovascular

In Summary:
  • According to Jeremy Hammond, numerous studies have indicated that the spike protein of "SARS‑CoV‑2" by itself, in the absence of whole viable "virus," can have pathogenic and toxic effects
  • However, the studies supplied do not use purified/isolated spike proteins but recombinant proteins which are a manipulated form of protein, which is generated in various ways to produce large quantities of proteins, modify gene sequences and manufacture useful commercial products
  • Recombinant protein is encoded by a gene — recombinant DNA — that has been cloned in a system that supports expression of the gene and translation of messenger RNA
  • In such cases the system in which the protein is expressed must be easy to culture and maintain, grow rapidly, and produce large amounts of protein
  • The various protein expression systems are:
    1. Bacteria
    2. Yeast
    3. Insect
    4. Mammalian
  • A few of Hammond's studies also relied on "pseudoviruses" which are a kind of recombinant "virus" with their core or backbone and surface proteins derived from different "viruses"
  • Genes inside "pseudoviruses" are usually altered or modified to abolish native surface protein expression
  • An additional plasmid is then used to express alternative surface proteins, producing a "pseudovirus" that can infect susceptible host cells but can only replicate intracellularly for a single round
  • As "viral" surface proteins are said to play pivotal roles in gaining entry into host cells, the conformational structures of "pseudoviral" surface proteins have high similarity to that of the native "viral" proteins; however, "pseudoviruses" have attenuated virulence compared with wild-type (WT) "viruses," allowing them to be safely handled in biosafety level 2 laboratories
  • "SARS-CoV-2" subunit S1 (RayBiotech, Cat No 230–01101)
  • "SARS-CoV-2" RBD (RayBiotech, Cat No 230–01102)
  • "SARS-CoV-2" subunit S2 (RayBiotech, Cat No 230–01103)
    • All three are recombinant "spike proteins" expressed in E. Coli and maintained in a filtered solution in 50 mM Na2HPO4 (pH 7.4), 0.5 M NaCl, 450 mM imidazole, and 6 M urea
  • "SARS-CoV-2 S1" (RayBiotech, Cat No 230–30161-10)
    • A recombinant "spike protein" grown in Human embryonic kidney 293 (HEK293) cells and supplied as a 0.2 um filtered solution in PBS (pH 7.4)
  • "SARS-CoV-2 S2" also derived from HEK293 cells were used in experiments where indicated
  • Other recombinant proteins (i.e TNFα) were purchased from R&D Systems (Minneapolis, MN, USA)
  • To test functional outcomes, two (a 2D and a 3D vessel-like) in-vitro models of the blood brain barrier (BBB) using primary brain endothelial cells were used
  • Primary human brain microvascular endothelial cells (hBMVECs) were isolated from fetal brain tissue
  • Cells were grown on rat tail collagen I coated flasks (BD Biosciences) in full growth medium (EBM-2 medium supplemented with EGM-2MV SingleQuots (Lonza, Cat No CC-3156 and CC-4147)) in an incubator set to 37 °C, 5% CO2, and 100% humidity and experiments were performed in the basal medium (EBM2 supplemented with 10% FBS)
  • These systems (when also coupled with other cells) represent the most advanced recapitulation (to reproduce or closely resemble) of the blood-brain barrier
  • These results suggest that whether free "viral" spike proteins or those on the surface of the "virus" present during "SARS-CoV-2" infection could induce barrier permeability (albeit once a certain threshold is reached) equivocal to the concentrations used here (i.e. these results only relate to the lab-created conditions and concentrations used for the study)
  • As this is the first report on the topic, they admit much work remains, particularly in regard to how permeability dynamics may change once these 3D microfluidic constructs are used with the whole "SARS-CoV-2 virus"
  • It was found that the treatment of cultured primary human pulmonary artery smooth muscle cells (SMCs) or human pulmonary artery endothelial cells with the recombinant "SARS-CoV-2" spike protein S1 subunit is sufficient to promote cell signaling without the rest of the "viral" components
  • In the cell culture experiments, two recombinant "SARS-CoV-2" spike proteins were studied
  • Cultured primary human pulmonary artery SMCs and human pulmonary artery endothelial cells were treated with these proteins for 10 min
  • They used the "phospho-specific" MEK antibody to determine that the recombinant full-length S1 subunit of "SARS-CoV-2" alone at a concentration as low as 130 pM, activated MEK
  • The authors claim that recent observations suggest that the "SARS-CoV-2" spike protein can by itself trigger cell signaling that can lead to various biological processes
  • Thus, they determined it is reasonable to assume that such events, in some cases, result in the pathogenesis of certain diseases
  • According to the authors, this protein may also affect the cells of systemic and coronary vasculatures, eliciting other cardiovascular diseases such as coronary artery disease, systemic hypertension, and stroke (i.e. it is pure speculation as there is no evidence of this)
  • In addition to cardiovascular cells, other cells that express ACE2 have the potential to be affected by the "SARS-CoV-2" spike protein, which may cause adverse pathological events (i.e. it is pure speculation as there is no evidence of this)
  • The authors state that it is important to consider the possibility that the "SARS-CoV-2" spike protein produced by the new "COVID-19" vaccines triggers cell signaling events that promote PAH, other cardiovascular complications, and/or complications in other tissues/organs in certain individuals (i.e. it is pure speculation as there is no evidence of this)
  • The researchers administered a pseudovirus expressing S protein (Pseu-Spike) to Syrian hamsters intratracheally (through the throat)
  • Lung damage was apparent in animals receiving Pseu-Spike, (i.e. fake-spike…granted that's an ironic admission as they all are) revealed by thickening of the alveolar septa and increased infiltration of mononuclear cells
  • The researchers admitted that the use of a noninfectious pseudovirus is a limitation to this study
  • However, they claim that their data revealed that (fake) S protein alone can damage endothelium, manifested by impaired mitochondrial function and eNOS activity but increased glycolysis
  • It appeared that (fake) S protein in ECs increases redox stress which may lead to AMPK deactivation, MDM upregulation, and ultimately ACE2 destabilization
  • They then admitted that their findings needed to be confirmed with the "SARS-CoV-2 virus" in the future study thus showing that their paper is utterly meaningless and irrelevant
  • Studying "SARS-CoV-2" can be challenging because experiments involving the intact "virus" requires a Biosafety Level 3 laboratory
  • To overcome this hurdle, the researchers created a new model of acute lung injury that utilizes transgenic mice (genetically-altered mice) that express the human receptor for "SARS-CoV-2" in their lungs
  • "Our mouse model dramatically reduces the danger of doing this type of research by allowing COVID-19 lung injury to be studied without using the intact, live virus"
  • The researchers injected the genetically modified mice with a segment of the spike protein and analyzed their response 72 hours later
  • The genetically modified mice injected with the spike protein exhibited "COVID-19-like" symptoms that included:
    1. Severe inflammation
    2. An influx of white blood cells into their lungs
    3. Evidence of a cytokine storm
  • Is injecting cultured goo down the throats of genetically altered mice not supposed to result in severe inflammation and increased WBC's in the blood?
  • Thus, they claim to have developed an acute lung injury model by intratracheally instilling the S1 subunit of "SARS-CoV-2" Spike S protein (400 µg/kg, 2 ml/kg body weight) in K18-hACE2 transgenic mice that overexpress the human receptor for "SARS-CoV-2" Spike protein S, ACE2, and investigated outcomes 72 hours later
  • They proposed that a single exposure of K18-hACE2 mice to "SARS-CoV-2" Spike Protein S subunit S1 may represent a valid model of "COVID-19," allow the study of the molecular mechanisms of "SARS-CoV-2" induced lung injury and be useful in the investigation of potential new therapeutic approaches to the management of "COVID-19" as well as future "coronavirus-dependent respiratory diseases"
  • No mention of how the spike protein was created/aquired but it was most likely yet again a recombinant protein due to the fact that the researchers were not using "intact live viruses" nor in need of a biosafety level 3 facility
  • Ultrasensitive single-molecule array (Simoa) assays were used for the detection of "SARS-CoV-2" antigens spike (S1–S2 unit), S1, and nucleocapsid and antibodies immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin M (IgM) against SARS-CoV-2 spike, S1, receptor binding domain (RBD), and nucleocapsid
  • One individual presented detectable S1 on day zero, possibly due to assay cross-reactivity with other human "coronaviruses" or asymptomatic infection at the time of vaccination
  • Spike protein was detectable in 3 of 13 participants an average of 15 days after the first injection
  • After the second vaccine dose, no S1 or spike was detectable, and both antigens remained undetectable through day 56
  • They observed an increase in S1 over an initial period of 1–5 days, suggesting that mRNA translation begins immediately after vaccine inoculation
  • Spike protein concentrations in plasma of vaccinated participants may be below the assay limit of detection
  • The researchers hypothesized that the cellular immune responses triggered by T-cell activation, which would occur days after the vaccination, lead to direct killing of cells presenting spike protein, and an additional release of spike into the blood stream
  • The mechanisms underlying release of free S1 and the subsequent detection of the intact spike protein remain unclear and require further studies
  • Limitations of the current study include the small sample size and potential biases that result from enrolling healthy, young adults, which may not be representative of the general population
  • Nonetheless, they concluded that the evidence of systemic detection of spike and S1 protein production from the mRNA-1273 vaccine is significant and has not yet been described in any vaccine study, likely due to limitations in assay sensitivity and timing assessment
  • In other words, results such as the ones presented here were likely never reported before due to the admitted limitations of the technology used
  • The clinical relevance of this finding is unknown and should be further explored
  • The spike proteins used were all lab-generated recombinant creations:
    1. "SARS-CoV-2" Spike protein (produced in Bing Chen's lab)
    2. Nucleocapsid recombinant protein (Ray Biotech 230-30164)
    3. S1 protein (Sino Biological 40591-V08H)
    4. RBD (produced in Aaron Schmidt's lab)
  • This commentary states that even in the absence of "SARS-CoV-2 virus," Spike glycoprotein alone causes endothelial damage and hypertension in vitro and in vivo in Syrian hamsters by down-regulating angiotensin-converting enzyme 2 (ACE2) and impairing mitochondrial function
  • The study cited by the authors as evidence for the spike protein being pathogenic alone was Hammond's previous study admitting to limitations of using a pseudovirus
  • They admitted that although these findings need to be confirmed in humans, the implications of this finding are staggering, as all vaccines authorized for emergency use are based on the delivery or induction of Spike glycoprotein synthesis
  • In the case of mRNA vaccines and adenovirus-vectorized vaccines, not a single study has examined the duration of Spike production in humans following vaccination
  • The authors state that under the cautionary principle, it is parsimonious to consider vaccine-induced Spike synthesis could cause clinical signs of severe "COVID-19," and erroneously be counted as new cases of "SARS-CoV-2" infections
  • They state that relying on a careful evaluation of the relevant scientific research, is urgent and that it is imperative to follow the science (both of which they obviously did not do)
  • While the authors are right in that the severe reactions from vaccines are attributed to "SARS-COV-2," they are promoting a fraudulent theory that a spike protein was created by the injection and is the cause
  • Although the mechanisms for development of myocarditis are not clear, several hypotheses have been proposed:
    1. Molecular mimicry between the spike protein of "severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)" and self-antigens
    2. Trigger of preexisting dysregulated immune pathways in certain individuals
    3. Immune response to mRNA, and activation of immunologic pathways
    4. Dysregulated cytokine expression
  • Antibodies against "SARS-CoV-2" spike glycoproteins have been experimentally shown to cross-react with structurally similar human peptide protein sequences, including α-myosin
  • The study cited within the review as evidence for the role the spike protein may have in causing myocarditis used recombinant "SARS-CoV-2" spike protein S1 and recombinant "SARS-CoV-2" nucleocapsid protein purchased from RayBiotech along with commercially made antibodies
  • Using digital droplet PCR, the researchers found that 36% (4 of 11) of severe "COVID-19" patients' PBMCs contained "SARS-CoV-2" RNA compared to 4% (1/26) of PASC patients' PBMCs
  • The one PASC patient that was RNA positive was 15 months post infection
  • They performed high parameter flow cytometry with antibodies that define B cell, T-cell, and monocytic subsets in addition to simultaneous staining of these cells with an antibody for the "SARS-CoV-2 S1" protein to find the reservoir of the RNA
  • To confirm the presence of "SARS-CoV-2" S1 protein (as they could not see it), they sorted CD14lo, CD16+ monocytes and performed Ultra High-Performance Liquid Chromatography (UHPLC)
  • After numerous preparation processes, the samples were then digested with AspN and LysC endopeptidases for 16h at 37°C
  • The digested peptides were analyzed on an Agilent 6550 IonFunnel QTOF and 1290 UHPLC by comparing patient samples to identical digests performed on commercially available "SARS-CoV-2" S1 subunit (a commercially made recombinant spike protein)
  • S1 subunit peptides from patient samples were mapped to a peptide database generated using commercial S1 subunit digests
  • The retention time of the representative peptide NLREFVFK in the digested commercial S1 subunit and Sample LH1-6 matched
  • Additionally, the Mass Spectra show identical mass, isotope distribution, and charge states for the representative peptide NLREFVFK in the representative LH1 sample and commercial S1 subunit
  • Using these metrics, up to 44% of the S1 subunit peptides could be identified in patient samples LH1-LH6 providing complementary evidence to flow cytometry experiments that demonstrate the presence of S1 subunit protein in these patient cells
  • As can be seen, they used indirect measurements of peptides matched between patient samples and recombinant spike proteins which were mapped to a peptide database created from the lab-created recombinant protein in order to claim INDIRECTLY that the spike protein was in the patients samples
  • Only fragmented "SARS-CoV-2" RNA was found in PASC patients
  • No full length sequences were identified, and no sequences that could account for the observed S1 protein were identified in any patient
  • They felt it was important to note that the S1 protein detected in these patients appeared to be retained from prior infection or phagocytosis of infected cells undergoing apoptosis and is not the result of persistent "viral" replication
  • Full length sequencing of the five cases submitted for genomic analysis failed to identify any full-length sequence in the spike protein gene, or any other gene, that could account for the observed spike protein detected by proteomic analysis
  • Aliquots 200 of peripheral blood monolayer cells were frozen in media that contained 90% fetal bovine serum and 10% dimethyl sulfoxide and stored at -70°C.
  • Cells were stained and analyzed using a 17-color antibody cocktail including a PE-labeled "SARS-CoV-2" S1 antibody
  • Retraction published on 10 May 2022, see Viruses 2022, 14(5), 1011
  • After publication, the first author contacted the editorial office regarding an improper experimental design with the potential to significantly affect the integrity of the resultant experimental data
  • Both the chosen construct of the spike plasmid that contained a C-terminal fused with 6xHis tag and use of a GFP reporter system under overexpression conditions in the protocol were identified as having the potential to introduce significant ambiguity regarding the nature of the reported observations
  • The reliability of the results and conclusions presented have therefore been undermined
  • Furthermore, statements regarding the effect of the spike protein on the adaptive immunity are misleading as in this article no experiments related to the adaptive immunity were performed, and the full-length spike-based vaccine was not studied
  • Therefore, conclusions related to vaccine safety are not validated and lacked experimental support
  • The authors claim that the results demonstrated the induction of circulating exosomes carrying the "SARS-CoV-2" spike protein by day 14, when Abs to the spike protein were not detectable in the sera using an ELISA method developed in their laboratory
  • Blood was collected before vaccination, days 7 and 14 after the first dose, day 14 after the second dose, and 4 mo after both the doses
  • They analyzed eight healthy adult volunteers (small sample size) vaccinated with the mRNA-based "SARS-CoV-2" vaccine (Pfizer–BioNTech)
  • Exosomes were "isolated" from 500 µl of plasma using Invitrogen Exosome Isolation Kit followed by 0.22-micron filtration
  • Development of Abs to "SARS-CoV-2" spike Ag was determined using an ELISA developed in their laboratory
  • In brief, 1 μg/ml "SARS-CoV-2" spike protein (a recombinant protein from Sino Biological) suspended in PBS was coated on an ELISA plate and incubated overnight at 4°C
  • Exosomes were labeled with immunogold and mouse "anti–SARS-CoV-2" spike Ab, and "coronavirus" FIPV3-70 Ab was added to the grids
  • They performed transmission electron microscopy using Abs specific for "SARS-CoV-2" spike to demonstrate the presence of "SARS-CoV-2" Ags on the surface of exosomes from controls and healthy vaccinated individuals
  • Exposure to the recombinant S protein alone elicited signalling and functional alterations
  • Cardiac PCs were immunosorted as CD31neg/CD34pos cells from human myocardial samples, and expanded in a dedicated medium supplemented with human recombinant growth factors and 2% v/v foetal calf serum (FCS)
  • Samples were finely minced using scissors and scalpel until nearly homogenous and digested with Liberase (Roche) for up to 1 h at 37 C, with gentle rotation
  • Human coronary artery ECs (CAECs) were purchased from PromoCell and expanded in the same medium used for PCs
  • Cells were used between passages 4 and 7
  • The human gut epithelial cell line, Caco2, expressing hACE2 and the African green monkey kidney cell line VeroE6 engineered to overexpress the human ACE2 and TMPRSS2 were also used
  • The presence of S protein in "COVID-19" patients' serum was evaluated using the "COVID-19" Spike Protein ELISA Kit from Abcam (ab274342), according to manufacturer's instructions (i.e. they used antibodies to indirectly claim the presence of the spike protein)
  • The antibody supplied in the kit (i.e. commercially made lab created antibodies) recognised the S2 domain
  • "SARS-CoV-2" S protein was expressed in insect cells
  • Secreted S protein was harvested 3 days after infection by centrifuging the cell culture at 1000×g for 10 min followed by another centrifugation of supernatant at 5000×g for 30 min
  • S protein-containing medium was incubated with HisPur Ni-NTA Superflow Agarose (Thermo Fisher Scientific) for 1 h at 4°C
  • Fractions containing the S protein were pooled (i.e. they were mixed together) and concentrated using 50-kDa MWCO Amicon centrifugal filter units (EMD Millipore)
  • Recombinant Spike S1 (#10522-CV) and S2 (#10584-CV) were purchased from R&D, resuspended in PBS according to manufacturer's instructions, aliquoted and stored at −80°C until use
  • Similarly to the S-ECD, the S1 and S2 proteins were produced in insect cells
  • The authors reported that two-third of patients tested did not have their PCs infected by "SARS-CoV-2," while the rate of infection was below 8% in the remaining subjects, suggesting a very low permissiveness of these cells to the "coronavirus," at least in vitro (in the lab)
  • Further investigation in a larger population of patients is warranted to determine the cause for the inter-individual variability in PC infection
  • They could not exclude that different scenarios may happen in vivo (in a living organism)
  • Low amounts of the S protein could be detected in pre-pandemic control sera
  • This could be explained by the sequence homology between some regions of the S protein and other human proteins/peptides (i.e. the S protein has the same sequences as human proteins/peptides)
  • Unfortunately, the immunogen sequence for this particular ELISA kit ab274342 is proprietary information, therefore they could not determine if it can recognise the S protein residues that have homology with unrelated peptides
  • The study was conducted on isolated cells and therefore the evidence must be confirmed in vivo (i.e. within a living organism)
  • The amount of S protein used for in vitro studies was higher than the average S protein concentration detected in "COVID-19" patients' serum (in other words, the researchers needed to use more S protein material than what is "seen" in regular patients in order to get the results they wanted)
  • The authors claim that circulating S protein represents the spill-over from infected organs, where concentration may be higher due to retention at the receptor level, however, as they did not have access to post-mortem myocardial samples, they could not verify this hypothesis
  • The researchers produced "SARS-CoV-2" Spike or VSV-G protein-pseudotyped "virions," or generated cells expressing Spike on their plasma membrane, and tested their effects on:
    1. Platelet adhesion (fluorescence)
    2. Aggregation (absorbance)
    3. Exposure of phosphatidylserine (flow cytometry for annexin V binding)
    4. Calcium flux (flow cytometry for fluo-4 AM)
    5. Clot formation and retraction
  • I was unable to highlight more from this study as it would not allow me to copy/paste but seeing as to how the experiments involved "pseudoviruses" and cell cultured creations, it's pretty safe to conclude that the results hold no relation to anything that would naturally occur within a living organism
  • The concept that the S protein can cause detrimental effects in "COVID-19" patients independent of infection could partially explain the long-term health issues
  • The author sites the study by Avolio et al. (discussed two sections above) and state that it provides strong evidence that the circulating S protein could be more detrimental to cardiac health than infection of "SARS-CoV-2" to the heart
  • More specifically, the S protein was found to act through the CD147 receptor on human cardiac pericytes to cause microvascular dysfunction
  • Avolio et al. also determined that the S protein caused human cardiac pericyte inflammation via yet to be determined mechanisms
  • The author admits that although the findings of the current study are provocative, future investigations need to expand the doses of S proteins to lower levels and other S protein variants for in vitro studies

Back in June 2020, CNN's very own Dr. Sanjay Gupta, of all people, wrote an article which warned the public to be wary of the flood of scientific studies coming out during the early days of the pandemic. The article was titled Science by press release: When the story gets ahead of the science and Dr. Gupta wrote about his observations after deciding to look at the available data pouring in from the scientific community. In his own assessment, he was "surprised at how thin the available data actually is in peer-reviewed medical journals." He rightfully pointed out that most of what was seen came in the form of press releases or pre-print reports that had not undergone the scientific scrutiny of independent review. In fact, Gupta stated that the studies being offered up and showcased were not ready for "prime time." He observed that many were not studies at all, but rather subjective conclusions based on data, and methods which remained hidden and difficult to validate. 

It seems that Jeremy Hammond must have missed this article by Dr. Gupta as his own "fact-check" of the "fact-checkers" is full of commentaries, preprints, unverified studies with hidden and faulty methods, and even one paper that was fully retracted more than a month before Hammond's own article was published. None of the studies supplied ever utilized any so-called spike proteins purified and isolated directly from human fluids. Instead, lab-created genetically engineered cloned and cultured recombinant concoctions grown in bacteria and insect cells and/or "pseudoviruses" created from similar cultured manipulations were used. The studies were done in artificial cultured conditions in vitro, i.e. in a petri dish in a lab, and the results could not be extrapolated to what occurs in vivo, i.e. within a living organism. Thus, any conclusions, hypotheses, and theories based off of the fraudulent data supplied from these studies amounts to nothing more than science fiction novels written by your favorite virologist, blogger, "fact-check," and/or media personality.

It does not matter how many studies someone like Hammond chooses to throw out in support of their argument if the studies themselves are built upon fraudulent foundations and have not been properly reviewed, reproduced, replicated, and verified. What ensues is an article spewing forth a preponderance of faulty evidence. This is a problem as, to the layperson, the numerous links and conclusions from the studies looks impressive upon first glance. This false narrative generated from deceitful practices helps to sell the idea that a spike protein exists and can be created from the mRNA injections in some fantastical unobservable process. It helps to keep the "virus" lie alive in that these researchers are able to work with, manipulate, and generate pieces of the invisible "virus" in order to study. It helps to keep the pharmaceutical lies alive in that there are "safer" therapeutics and drugs available that can specifically target the spike protein of the fictional entity. It helps to keep confidence and belief in pseudosciences like genomics said to identify and recreate the protein through recombination as well as immunology in order to tag these invisible entities with fictional antibodies and determine indirectly how the body responds to them. It helps to keep the confused, who are looking for a way out of the germ theory and pharmaceutical lies, entrenched into this deceptive web of disinformation and misrepresentation.

There is no need to create a hypothetical narrative around a fictional spike protein in order to claim how the mRNA vaccines harm a person. The very act of injecting anything into the body is a potential cause of harm as this is an unnatural way for the body to encounter any substance. Even injecting something as simple as water can cause disruption of red blood cells as well potential kidney damage. The "vaccines" are full of contaminants both known and unknown and people who are allowing the injection of these substances into their bodies are playing Russian Roulette with their own health. No fictional spike protein is necessary to explain the harm these injections can cause. People like Jeremy Hammond are doing nothing more than perpetuating fear founded upon unscientific fraud.

ViroLIEgy
15 Jul 2022 | 1:49 pm

The No “Virus” Challenge


Over the past few weeks, I have had the privilege of working with some brilliant people on establishing a challenge to virology in order to finally put their (pseudo)scientific methods to the test. Stemming from the mind of Dr. Tom Cowan and meticulously crafted by Dr. Mark Bailey and Dr. Kevin Corbett, the No "Virus" Challenge is designed to meet virology halfway. We want virology to show us, using their own methods, that they can actually independently reproduce and replicate the exact same results while blinded to the different samples that they will be working with.

I will leave the exact details of the challenge to be explained by the document linked below, but we are offering a first step to finally settle this debate once and for all. Whether the virology community (and those who back them) will accept this challenge (which Dr. Cowan has already received financial backing for) remains to be seen. However, if the virologists are truly interested in science and performing the proper control experiments that should have been carried out from the very beginning, there is absolutely no reason for them not to accept.

SETTLING THE VIRUS DEBATE – SourceDownload

Source Document: https://drsambailey.com/resources/settling-the-virus-debate/

Dr. Tom Cowan discussed in detail the No "Virus" Challenge with Dr. Mark Bailey on his YouTube channel which you can watch below.

ViroLIEgy
12 Jul 2022 | 5:38 pm

The Spike Protein


I often get asked many questions regarding the so-called "coronavirus" spike protein, such as whether or not it actually exists and whether it is actually in the vaccine. Does this particle hold any biological relevance whatsoever or is it just another in a long line of illustrations used to generate fear? If anyone is unaware at this point, the spike protein is said to be the 9-12 nm protrusions seen in TEM images of the "virus" which gives it the spiked or "corona" appearance around the outside edges. According to mythology, these proteins allow the "virus" to penetrate the host cell and begin the infection process. The spike protein has risen to prominence due to the continued propaganda around the mRNA vaccines which are claimed to produce the spike in the body once injected. This is said to trigger an immune response which teaches the body how to prepare an army of antibodies to fight off any sneaky stealh variant…or not. It depends on the variant, the manufacturer, the dose, the schedule, the disease outcome, etc.

According to the WHO:

"Evidence on vaccine effectiveness (VE) against symptomatic illness and severe disease is expected to become available only when variant-updated vaccines have been introduced into broader use."

"Currently available COVID-19 vaccines are based on the index virus (also referred to as the ancestral strain); however, there has been continuous and substantial SARS CoV-2 viral evolution, particularly in the spike (S) protein.  These genomic changes in the virus have resulted in several VOC that have circulated in waves, with varying degrees of immune evasion, some of which have resulted in lower VE of existing COVID-19 vaccines compared to the initial VE against the index virus. The magnitude of the reduction in VE varies by product, schedule, disease outcome, VOC and time since last dose. From January to June 2022, the dominant SARS-CoV-2 variant globally has been the Omicron variant, with emergence of additional sub-lineages (1). The Omicron variant is the most antigenically distinct variant from the index virus and has exhibited the highest degree of immune evasion to current COVID-19 vaccines, compared to the index virus. Current vaccines continue to perform well in preventing severe disease and death due to Omicron, particularly with the use of a booster dose(s). However, protection against infection and symptomatic illness due to the Omicron variant is lower than other variants and declines rapidly, even after a third (booster) dose.  Those at highest risk for severe disease, hospitalization, and death remain older persons, those with comorbidities and immunocompromising conditions, and other vulnerable populations as described in the WHO Prioritization Roadmap (2)."

https://www.who.int/news/item/17-06-2022-interim-statement-on-decision-making-considerations-for-the-use-of-variant-updated-covid-19-vaccines

The WHO states that the failure of the vaccines is due to the continual and rapid changes to the spike protein as it evolves and evades the immune systems defenses. This amazing super power has left us exactly in the same state we were in before the use of the toxic jabs over two years ago: the "virus" is still running rampant, the 99% of the population that were never at risk remain not at risk, and those who were at an increased risk of disease remain so. However, now we have many who are needlessly being injured by a vaccine never proven to be safe and effective with no data on long-term safety. It is clear that there was never any protection offered by the vaccine. The story created around the way the theoretical spike protein supposedly works is nothing but pure fiction attributed to an unobservable process said to occur inside the body after injection.

According to the CDC:

"To trigger an immune response, many vaccines put a weakened or inactivated germ into our bodies. Not mRNA vaccines. Instead, mRNA vaccines use mRNA created in a laboratory to teach our cells how to make a protein—or even just a piece of a protein—that triggers an immune response inside our bodies. That immune response, which produces antibodies, is what helps protect us from getting sick from that germ in the future.

  1. First, mRNA COVID-19 vaccines are given in the upper arm muscle. After vaccination, the mRNA will enter the muscle cells. Once inside, they use the cells' machinery to produce a harmless piece of what is called the spike protein. The spike protein is found on the surface of the virus that causes COVID-19. After the protein piece is made, our cells break down the mRNA and remove it.
  2. Next, our cells display the spike protein piece on their surface. Our immune system recognizes that the protein does not belong there. This triggers our immune system to produce antibodies and activate other immune cells to fight off what it thinks is an infection. This is what your body might do if you got sick with COVID-19.
  3. At the end of the process, our bodies have learned how to help protect against future infection with the virus that causes COVID-19. The benefit is that people get this protection from a vaccine, without ever having to risk the potentially serious consequences of getting sick with COVID-19. Any side effects from getting the vaccine are normal signs the body is building protection."

https://www.cdc.gov/coronavirus/2019-ncov/vaccines/different-vaccines/mRNA.html?s_cid=11344:how%20does%20mrna%20vaccine%20work:sem.ga:p:RG:GM:gen:PTN:FY21

Fortunately for the WHO and the CDC, they have the convenient rescue device of "continued and rapid evolution" to explain away the contradictions and failures of the vaccines said to be based on this fictional piece of an imaginary "virus." They want you to believe that the vaccines will never be 100% effective as long as the spike protein can magically change itself inside the comput…er, body. Thus, newer and better vaccines created for the evolved spike protein along with regular boosters will be needed to combat the elusive nature of this highly intelligent protein endowed with shape-changing super powers. Any failures are due to the evolving particle, not the fraudulent approach.

Obviously, there are quite a few problems with this story beyond the inability to observe the fictional spike protein production process play out inside a living organism as well as the fantastical evolutionary powers of this tiny protein. If one were to think about this critically and logically, one would ask the same questions that should be asked about the evidence for the existence of any "virus." How was this spike protein discovered? Has this protein ever been observed in nature? Was it purified and isolated directly from the fluids of sick humans or was it a creation of the cell culture process? How was its functioning determined? Were proper controls carried out in any of the studies?

It should be clear to anyone who has ever looked into the original papers supplied as evidence for the "coronaviruses" that the spike protein is nothing but a creation based off of the staining patterns of random particles chosen as the representation for the alleged "virus." Sometimes these spikes appear in the electron microscope images and other times they do not (even though they are said to be there):

Discernible spikes?!?! "Spikes of SARS-CoV-2 particles observed on the cell surface were discernible" https://www.nature.com/articles/s41598-020-73162-5/figures/2

If the spikes are not observed, sometimes the sample is manipulated until they appear such as was done in this recent "SARS-COV-2" study from Australia where trypsin, a protein digestor, was added to alter the appearance of the imaged particles so that they contained the spikes:

"Electron micrographs of the negatively stained supernatant showed spherical and pleomorphic virus‐like particles of 90–110 nm diameter; the particles displayed prominent spikes (9–12 nm), characteristic of viruses from the family Coronaviridae (Box 5, A). Electron micrographs of sectioned VERO/hSLAM cells showed cytoplasmic membrane‐bound vesicles containing coronavirus particles (Box 5, B) Following several failures to recover virions with the characteristic fringe of surface spike proteins, it was found that adding trypsin to the cell culture medium immediately improved virion morphology."

There seem to be quite a few unstained spikeys floating off there by themselves…

https://www.mja.com.au/journal/2020/212/10/isolation-and-rapid-sharing-2019-novel-coronavirus-sars-cov-2-first-patient

One thing that is for certain in the case of the creation of these spiked proteins is that the particles observed do not come from purified and isolated "viruses" found directly in the fluids of sick organisms. In fact, they are not even specific to "coronaviruses" at all as they can be observed on many extracellular vesicles such as clathrin-coated vesicles and exosomes:

Spikes on exosomes!!! doi: 10.1016/0092-8674(83)90040-5

Even the 2009 H1N1 swine flu gets some spiked love:

https://www.sciencephoto.com/media/83724/view/2009-h1n1-swine-flu-virus-tem#

The particles claimed to be spike proteins are a creation stemming from the cell culture process used to "isolate" the "viruses" as well as the preparations done in order to obtain the images by way of electron microscopy. As Harold Hillman said, the images obtained at the end of the process are far away removed from realty:

"For example, most cytologists know, but readers of elementary textbooks do not, that when one looks at an illustration of an electron micrograph: an animal has been killed; it cools down; its tissue is excised; the tissue is fixed (killed); it is stained with a heavy metal salt; it is dehydrated with increasing concentrations of alcohol; it shrinks; the alcohol is extracted with a fat solvent, propylene oxide; the latter is replaced by an epoxy resin; it hardens in a few days; sections one tenth of a millimetre thick, or less, are cut; they are placed in the electron microscope, nearly all the air of which is pumped out; a beam of electrons at 10,000 volts to 3,000,000 volts is directed at it; some electrons strike a phosphorescent screen; the electron microscopists select the field and the magnification which show the features they wish to demonstrate; the image may be enhanced; photographs are taken; some are selected as evidence. One can immediately see how far the tissue has travelled from life to an illustration in a book."

https://www.big-lies.org/harold-hillman-biology/what-price-intellectual-honesty.htm

It should be clear that if none of the "coronaviruses" (ranging in size from 60 to 150 nm) have ever been properly purified, isolated, and separated from everything else in order to be independently studied, the much smaller surface spikes of the "virus" (ranging from 9 to 12 nm) have also never been properly purified and isolated in order to be independently studied. To confirm this, I did some digging into just the so-called purification and isolation procedures relating to the spike itself. I came across a book by David Cavanagh, a man intimately tied to the study of this protein. He was involved in researching the "coronavirus infectious bronchitis virus (IBV)," focusing on the identification and molecular characterisation of the "virion" proteins. In his book, he laid out the foundational papers for its supposed purification and isolation:

The Coronavirus Surface
Glycoprotein

A. Electron Microscope Observations

"Coronaviruses are frequently claimed to have a characteristic morphology, including the possession of a "club-shaped" surface projection or spike (S) glycoprotein. However, in common with other aspects of the coronaviruses, the group exhibits variation with respect to the shape, size, and distribution of the S protein on the virion surface. Davies and Macnaughton (1979) described the spikes of infectious bronchitis virus (IBV) and human coronavirus (HCV) 229E as being "tear-drop" shaped and widely spaced, whereas those of murine hepatitis virus (MHV) type 3 were mostly "cone-shaped" and closely spaced, although in some MHV-3 preparations the spikes were more bulbous. Dimensions of S vary not only among the coronaviruses but also depending on the staining procedure; following potassium phosphotungstate staining all three
viruses had spikes approximately 20 nm long and 10 nm wide at the bulbous end, except for the cone-shaped spikes of MHV, which had a diameter of only 5 nm (Davies and Macnaughton, 1979). The entire S protein has been observed after solubilization and purification (Sturman et 01., 1980; Cavanagh, 1983c). The nonenvelope-associated SI subunit of the IBV S protein can become detached from the virion (Stern and Sefton, 1982a; Cavanagh and Davis, 1986).

B. Sedimentation Characteristics

Purification of the S protein of MHV, IBV, HCV strain 229E, bovine coronavirus (BCV), and porcine hemagglutinating encephalomyelitis virus (HEV) has been achieved using a combination of nonionic detergent and sucrose gradient centrifugation (Sturman et a1., 1980; Hasony and Macnaughton, 1981; Cavanagh, 1983b; Schultze et a1., 1990, 1991). When milligram quantities of IBV were used, it was neeessary to dissociate and sediment the virus proteins in the presence of 1 M NaCI; otherwise the M protein cosedimented with S (Cavanagh, 1983b). Spike has also been purified by affinity chromatography (Mockett, 1985; Daniel and Talbot, 1990). Sedimentation studies have been variously interpreted as indicating that S from virions is a homodimer or homotrimer (IBV: Cavanagh, 1983eL homodimer (MHV: Vennema et a1., 1990b), or homotrimer (TGEV: Delmas and Laude, 1990)."

Click to access 10.1007%2F978-1-4899-1531-3_5.pdf

It is not my intention to completely deconstruct each of the purification/isolation papers listed as it seems rather ridiculous to do so when the "viruses" these spike proteins supposedly come from have never been scientifically proven to exist. However, I do want to share some brief highlights from each paper so that it is abundantly clear the amount of manipulations and alterations that the sample must be put through in order to get the desired results. These "proteins" stem from the unpurified cell culture process where many substances are added and nothing is isolated. It will be clear to see how far removed from reality the sample has travelled in order to become an image published in a study. It stretches beyond belief to assume that the representative particles, imaged in a heavily altered dead and fixed state, have any bearing on actual biological processes. They are nothing but a creation from the numerous processes utilized in order to obtain the final results.

1980

First up is the initial spike protein purification and isolation paper presented as evidence by Cavanagh. I highlighted the full methods section from this study in order to showcase the numerous steps involved to get to the final outcome. Many of the ensuing papers follow similar procedures in order to generate their outcomes so feel free to dig into each for more detailed accounts of the pseudoscientific processes employed.

What you will see in this paper is that the "virus" is a cell culture creation supplemented with the usual medium along with fetal bovine serum and antibiotics. The fetal bovine serum itself is a source of foreign genetic material along with other substances and compounds. The cell line used was the murine fibroblast cell line 17Cl-1, which, according to BEI Resources, was "derived by spontaneous transformation of 3T3 cells. 3T3 is a nontumorigenic cell line established from 14- to 17-day-old embryos of the Balb/c mouse strain. 17Cl-1 cells are used for cultivation of murine coronaviruses, including murine hepatitis virus." Thus, we can see that this is already an unpurified concoction.

After culturing the "virus," it was "harvested" from the sample before significant amounts of cytopathic changes such as cell fusion or lysis had occurred (the very criteria used to determine a "virus" is present) and then it was centrifuged. The sample was precipitated by the addition of 5.0 g of NaCl per 150 ml of clarified supernatant followed by a half volume of 30% polyethylene glycol. The "virus" was then put through a series of centrifugation steps with different chemicals and it was eventually radiolabeled with a uridine and amino acid mixture. NP40 was added to disrupt the "virions." According to this manufacturer, NP40 is a "non-ionic surfactant useful for the isolation and purification of functional membrane protein complexes. This detergent has been purified to reduce levels of contaminating aldehydes, metals, peroxides, and salts." In other words, more contaminants/foreign substances were added to "purify/idolate" the proteins.

Afterwards, the sample was subjected to the usual electron microscopy preparation procedures. The sample was also put through gel electrophoresis with a slew of additional treatment-mixture chemicals and then charged under high voltage for 4 hours in order to separate the proteins. Eventually, the researchers used theoretical antibodies created in similar unpurified manners to label and claim that the particles observed were the spiked ones that they were searching for. As is usually the case, no proper controls were outlined in this study:

Isolation of coronavirus envelope glycoproteins and interaction with the viral nucleocapsid

"Studies of the virion polypeptides of a number of different coronaviruses in several laboratories have led to reports of three to a dozen or more polypeptide species associated with virions (1, 3, 7, 11, 16, 19, 23, 24, 28-31, 33,35, 44, 45, 48; 0. W. Schmidt and G. E. Kenny, Fed. Proc. 38:910, 1979). The reasons for the apparent diversity in the polypeptide patterns of coronaviruses are not fully understood. Differences in technique and imperfect discrimination of virion polypeptides from those of host origin may account for some of the disparities. However, even when the same gel systems and conditions are employed in the same laboratory, significant differences in the number and size of virion polypeptides of different coronavirus strains have been observed (30). We propose that some of this apparent dissimilarity in the polypeptide patterns of coronaviruses may be the result of unusual characteristics of their envelope glycoproteins."

MATERIALS AND METHODS

"Cells and virus. A spontaneously transformed derivative of the BALB/c 3T3 cell line, designated 17 Cl 1, and the L2 derivation of the L929 cell line were grown in Dulbecco medium supplemented with 10% unheated fetal bovine serum, penicillin (100 U/ml), and streptomycin (100 ,ug/ml). The A59. strain of mouse hepatitis virus was produced in 17 Cl 1 cells and assayed by plaque titration in L2 cells as described previously (46).

Virus production and purification. 17 Cl 1 cell monolayers in glass roller bottles (120 by 260 mm; 690-cm2 cell surface area) were inoculated with A59 virus at a multiplicity of 1 to 10 PFU/cell. After an adsorption period of 1 h at 37°C, 50 ml of Eagle minimal essential medium with 10% unheated fetal bovine serum was added to each roller bottle. Cells were incubated at 37°C.

Released virus was usually harvested 24 to 26 h after inoculation, after several cycles of infection, when high yields were obtained and well before significant amounts of cytopathic changes such as cell fusion or lysis had occurred. Released virus was centrifuged at 10,000 x g (average) in a Sorvall GSA rotor for 30 min at 4°C to remove debris. For optimal preservation of virus infectivity, freshly harvested virus was purified immediately at 4°C without freezing or storage.

The virus was precipitated by the addition of 5.0 g of NaCl per 150 ml of clarified supernatant followed by a half volume of 30% polyethylene glycol to give a final concentration of 10% polyethylene glycol and 2.2% NaCl. The precipitate was collected by centrifugation at 10,000 x g (average) for 30 min at 4°C, resuspended in TMEN 6 buffer (5 ml/3 roller bottles of original virus) containing 0.05 M Tris-maleate-0.001 M EDTA-0.1 ml NaCl (pH 6.0) at 4°C, and layered over a discontinuous gradient of 4 ml of each of 30 and 50% (wt/wt) sucrose in TMEN 6 buffer in a 17.5-ml centrifuge tube or 3 ml of 30% and 2 ml of 50% (wt/wt) sucrose in TMEN 6 in a 12.5-ml centrifuge tube. After centrifugation for 4 h at 25,000 rpm in a Spinco SW 27.1 rotor (82,000 x g, average) or 3 h at 30,000 rpm in a Spinco SW 41 rotor (110,000 x g, average) at 4°C the narrow white virus band at the interface between 30 and 50% sucrose was collected, diluted 2.5-fold with TMEN 6 buffer, and layered over a 7.5- or 12-ml continuous gradient of 20 to 50% sucrose in TMEN 6 buffer. This gradient was centrifuged for 18 h at 25,000 rpm (82,000 x g, average) at 4°C on a Spinco SW 27.1 rotor or 30,000 rpm in a Spinco SW 41 rotor (110,000 x g, average), and the virus band at 1.17 to 1.19 g/ml was collected. The virus was then diluted with TMEN 6 buffer and either used directly, pelleted in an SW 50.1 Spinco rotor, or dialyzed against buffer or water. Data from a representative virus purification (Table 2) shows a 50- to 100-fold reduction in volume and greater than 100-fold decrease in total protein, with 60 to 100% recovery of virus infectivity. The final specific infectivity achieved was 5 x 10'0 to 10 x 1010 PFU/ml of protein.

As a routine practice, up to 900 ml of virus was purified at one time. This is the volume obtained from 18 roller bottles of infected cells. Virus harvested at 24 h had a titer of 2 x 10^8 to 5 x 10^8 PFU/rnl, and at 42 to 48 h the titer was 0.5 x 10^9 to 2 x 10^9 PFU/ml. Thus, depending on the time of harvest, yields of released virus were 10^10 to 10^11 PFU/roller bottle.

Radiolabeling of virus. Radiolabeled compounds were added to the medium in final concentration of 2 to 4 uCi of L-3H-amino acid mixture, or [5-3H]uridine per ml, 3 uCi of [6-3H]fucose per ml, and 1 to 4 uCi of [35S]methionine per ml. Infected cultures were incubated in the presence of these compounds from approximately 1 h after virus inoculation until virus was harvested. Labeled uridine and amino acid mixture were purchased from New England Nuclear Corp., Boston; labeled methionine and fucose were obtained from Amersham Corp., Arlington Heights, Ill [3H]-uridine-labeled 28S HeLa cell rRNA was kindly provided by N. K. Chatterjee.

Disruption of virions with NP40. Purified virions from three or fewer roller bottles were usually pelleted and resuspended in 1 to 2 ml of TMEN 6 buffer at 4°C. NP40, kindly provided by Shell, Inc., was added to a final concentration of 0.25 to 1%, and the mixture was shaken vigorously by hand at least 20 times. In some experiments a portion of the detergent-treated virus was incubated at 37°C for 30 min at this stage. The detergent-treated virions were then layered at 4°C over 15 to 50% sucrose gradients in TMEN 6 buffer containing 0.1% NP40 or at 10°C over 30 to 75% sucrose gradients in TMEN 6 buffer containing 0.1% NP40. A cushion of 76% Renografin or 65 to 75% sucrose was placed beneath the 15 to 50% sucrose gradient. Unless otherwise indicated, the gradients were sedimented at 38,000 rpm (180,000 x g, average) for 16 to 20 h in an SW 41 rotor at 4 or 10°C. Gradient fractions were collected from the top of the gradient with an ISCO fractionating device or from the bottom by displacement with light paraffin oil delivered with a Cornwall syringe. Gradient fractions were collected into chilled tubes and held at 4°C. Samples for radioisotopic counting were prepared by transferring 50- to 450-pd portions of each gradient fraction into 1 ml of water-10 ml of Aquasol (New England Nuclear). The refractive indexes of gradient fractions were determined with a Bausch and Lomb Abbe refractometer. Continuous 20 to 50% gradients of Renografin-76 (E. R. Squibb & Sons, Princeton, N.J.) containing 0.1% NP40 were employed for dissociation of nucleocapsid complexes. Sedimentation was carried out at 25,000 rpm (82,000 x g, average) for 16 h in an SW 27.1 rotor at 4°C.

Electron microscopy. Samples of purified glycoprotein preparations were placed on carbon-coated Formvar-covered 400-mesh copper grids, negatively stained with 2% phosphotungstic acid at pH 7.2 and examined with a Philips 400 transmission electron microscope.

SDS-polyacrylamide gel electrophoresis. The method of high-pH discontinuous buffer SDS-polyacrylamide gel electrophoresis in cylindrical gels employed in this study has been described previously (44). Because the El polypeptide aggregates after boiling with SDS in the presence of mercaptoethanol (44), samples of viral polypeptides for this study were prepared for electrophoresis by heating at 37°C for 30 min in the absence of mercaptoethanol. Five to twenty percent polyacrylamide gradient slab gels 1.5 mm thick and 10 cm long were prepared by the method of Laemmli in a Hoeffer slab gel electrophoresis apparatus. Each well was loaded with approximately 40 ul of a radiolabeled sample which had been heated to 37°C for 15 min with an equal volume of sample treatment mixture composed of 6 M urea, 4% SDS, 0.05% bromophenol blue in 0.0625 M Tris-chloride, pH 6.7. Gels were run at 125 V for about 4 h under constant voltage from a Savant power supply. Gels were impregnated with PPO (2,5-diphenyloxazole; Sigma) in dimethyl sulfoxide by the method of Bonner and Laskey (4), dried with a Savant gel drier onto Whatman no. 17 chromatography paper, exposed to Kodak XR-5 film at -70°C for 1 to 4 weeks, and developed with Kodak X-ray chemicals.

Preparation of antisera. Antiserum directed against A59 virion polypeptides were prepared by purifying released virus through discontinuous and continuous sucrose gradients as described above without prior precipitation with PEG. Purified, concentrated A59 virus was disrupted with 1% NP40 and frozen at -75°C in aliquots. A 0.1-ml amount of the virus preparation was inoculated with complete Freund adjuvant into rabbit footpads, followed after 2 weeks with a second footpad injection of an additional 0.1 ml with incomplete Freund adjuvant (Difco) and 1 week later by an intravenous injection of another 0.4 ml of detergent-treated virus. After the third injection, rabbits
were bled from the ear at 1-week intervals for 1 month. This antibody specifically immunoprecipitated radiolabeled El, N, and E2 and no cellular polypeptides from NP40 extracts of infected 17 Cl 1 cells.

Antisera against the isolated El and E2 proteins were prepared by a similar schedule of rabbit inoculations of El obtained from sucrose gradient sedimentation of A59 virions disrupted with NP40 at 4°C and of E2 from NP40-disrupted virus that had been incubated at 37°C before sucrose gradient sedimentation. These antisera were each passed through immunosorbent columns of Affigel 10 charged with the other viral glycoprotein. The specificity of the antisera was determined by immunoprecipitation of radiolabeled viral polypeptides from NP40 extracts of A59-infected cells.

Immunoprecipitation of viral polypeptides. Immunoprecipitates of radiolabeled viral polypeptides
from extracts of infected cells, purified virions, or gradient-purified El or E2 were made by the method of Kessler (26). A 25-ul amount of rabbit serum was incubated with 25 to 200 ul of radiolabeled sample in phosphate-buffered saline containing 0.1% NP40 at 0°C for 1 h. Antigen-antibody complexes and antibody were precipitated with an excess of purified, Formalin-fixed staphylococci (Cowan 1 strain) for 10 min at 4°C, pelleted at 3,000 rpm for 10 min, washed three times in 1 ml of 0.05% NP40 with phosphate-buffered saline and then solubilized in sample treatment mixture by boiling for 1 min or treatment at 37°C for 15-30 min."

The spike proteins in the bottom image created the exact same circle and spike pattern as in the original "viral" particle. That couldn't be a result from the procedures now could it…? 🤔
"The experimental evidence obtained here and in previous studies suggests a model for the arrangement of components in the coronavirus A59 virion (Fig. 11)."

doi: 10.1128/JVI.33.1.449-462.1980

1981

This next study followed similar procedures as the first. I've highlighted the "virus" growth and "purification" methods in order to show that this purification/isolation claim does not hold up under scrutiny. The "virus" was grown in mouse embryonic fibroblasts and incubated in Eagle's minimal essential medium with fetal calf serum. The "virus" was centrifuged and "purified" by methods "previously discussed." The rest of the techniques used are similar to those listed in the 1981 study and the results are heavily reliant on serological data where it was apparently difficult to ensure similar antibody responses in the mice tested as there was considerable variation observed. No EM images of the "purified/isolated" spike proteins accompany the study:

Antigenieity of Mouse Hepatitis Virus Strain 3  Subeomponents in C57 Strain Mice

Materials and Methods

Virus Growth 

"MHV3 was grown in confluent secondary mouse embryonic fibroblasts. Monolayers were infected at an input multiplicity of 0.1 infectious particles per cell and following an adsorption period of 1.5 hours at 37 ° C, were incubated for 72 hours at 37 ° C in Eagle's MEM with 2 percent foetal calf serum (13). Aliquots of this virus suspension were stored at –70°C and used for the preparation of purified virus particles and subcomponents. 

Preparation of Purified Virus 

Virus was purified at 0 ° to 4 ° C as described previously (13). The virus was pelleted at 75,000 × g for 1 hour and then resuspended in 1 ml Dulbecco's phosphate buffered saline "A" (PBSA). The resuspended virus was overlaid on to a linear 25 to 55 percent (w/w) sucrose gradient in PBSA and centrifuged for 16 hours at 90,000 × g. The virus peak at 1.18 g/ml was collected."

Diseussion

"In this paper we report the isolation and purification of MHV 3 subviral components and have shown the role of each subcomponent in the protection of immnnised mice against challenge with infectious MHV 3. It was difficult to ensure that mice immunised with different virus subcomponent preparations all produced comparable amounts of antibody, as there was considerable variation in the immunogenieity of the subeomponents. The highest antibody rises detected by ELISA were directed against surface projections, while lower antibody rises were observed against membrane and RNP, suggesting that the most immunogenic part of the virus is an antigen(s) associated with the surface projections. Similar results have been obtained previously with human eoronaviruses (14) and the porcine coronavirus transmissible gastroenteritis virus (TGEV) (5)."

doi: 10.1007/BF01315263.

1983

In this study, the "virus" was grown in the chorioallantoic membrane (CAM) cells of de-embryonated chicken eggs and radiolabelled IBV-M41 was prepared in pairs of de-embryonated eggs and treated. The same ultracentrifugation of impure cultured material was utilized to claim purity and isolation even though it is well known that this technique can not separate particles of the same size, shape, and density from one another. It is admitted in the study that there is less agreement among researchers on the composition of the S protein. It was also admitted that other polypeptides of 110K and 75K were detected in "virus" preparations which they assumed were probably host polypeptides. No EM images of the purified and isolated particles accompanied the study nor were proper controls carried out:

Coronavirus IBV: Further Evidence that the Surface Projections are
Associated with Two Glycopolypeptides

"The avian infectious bronchitis virus (IBV) particle, like other coronaviruses, contains three
major protein structures, the surface projection or peplomer (S), nucleocapsid (N) and matrix (M) proteins (Cavanagh, 1981 ; Siddell et al., 1982). The M protein comprises a polypeptide of mol. wt. 23 000 (23K) which is glycosylated to different extents to form glycopolypeptides of mol. wt. up to 36K (Stern et al., 1982; Stern & Sefton, 1982; Cavanagh, 1983). A polypeptide of 50K to 54K forms the N protein (Macnaughton et al., 1977). There is less agreement on the composition of the S protein. Since the presumptive S polypeptides of all coronaviruses examined have mol. wt. greater than that of the N polypeptide, the following account refers only to such IBV polypeptides."

"Radiolabelled IBV-M41 was prepared in pairs of de-embryonated eggs (Cavanagh, 1981); each egg received 125 uCi [35S]methionine (sp. act. > 800 Ci/mmol) or [35S]methionine plus 165 uCi of a mixture of 15 3H-labelled amino acids (code TRK 440, Amersham International). Unlabelled virus was grown in batches of 200 11-day-old embryonated eggs which were inoculated with approx. 3-5 log10 median ciliostatic dose50 of IBV-M41. After 24 h at 37 °C the eggs were chilled at 4 °C overnight. Allantoic fluid was collected, clarified at 4000 g for 30 min and the virus pelleted at 35000 g for 2-5 h. The pellet was resuspended in NET buffer (100 mM- NaC1, 1 mM-EDTA, 10 mM-Tris-HCl pH 7.4) to a vol. of 20 ml and sonicated at maximum amplitude for 10 s with the 3 mm probe of an MSE ultrasonic disintegrator. The suspension was placed on two discontinuous gradients comprising 20 m125% (w/w) sucrose and 5 m160% (w/w) sucrose in NET in a 6 x 38 MSE swing-out rotor. After centrifugation at 65,000 gmax for 2.5 h at 4 °C, the gradients were fractionated. Fractions which contained virus at the 25/60% sucrose interphase were pooled, diluted threefold, placed on a 25 to 55 % (w/w) sucrose gradient in NET and centrifuged at 50000 gay for 16 h at 4 °C in a 6 x 38 rotor. Fractions of 1 ml were collected and those of density 1.16 to 1.22 g/ml were pooled, diluted to 20% (w/w) sucrose and the virus pelleted at 90000g for 3 h at 4 °C in an MSE 3 x 25 swing-out rotor. Pelleted virus (2 to 4 mg protein) was resuspended in 1 ml I M-KCI or 1 M-NaC1 in NET and 1 ml 4% (v/v) Nonidet P40 (NP40) in NET containing 1 M-KCI or 1 M-NaCI, followed by sonication for 2 to 3 s and incubation at 25 °C for 1 h. Undissolved material was removed by low-speed centrifugation and the supernatant placed on a 10 to 55% (w/w) sucrose gradient in NET containing 1 M-KC1 or 1 M-NaC1 and 0.1 ~ NP40. After centrifugation in an MSE 6 x 38 swing-out rotor at 85,000 gav for 16 h at 4 °C fractions of 500 pi were collected. These were dialysed to remove KCI where appropriate prior to electrophoresis. SDS-polyacrylamide gel electrophoresis (SDS-PAGE) was performed in tubes and slabs with a 10% acrylamide resolving gel (Cavanagh, 1981). Samples were dissociated at room temperature with 2% SDS and 2% (v/v) 2-mercaptoethanol. Unlabelled markers used were phosphorylase b, bovine serum albumin and carbonic anhydrase; some phosphorylase was pre-stained with Drimarine brilliant blue K-BL (Bosshard & Datyner, 1977) and the apparent mol. wt. was 110K."

"Thus, these studies show that the peplomers of IBV comprise two glycopolypeptides of 90K and 84K in equimolar proportion. The polypeptides of 110K and 75K, variably detected in virus preparations, are probably host polypeptides."

doi: 10.1099/0022-1317-64-8-1787.

1985

In this study, affinity chromatography was used to "purify" cell cultured "viruses." However, keep in mind that it is known that this technique can not separate "viruses" from exosomes or other particles with the same size, shape, and density. The researchers also rely on theoretical monoclonal antibody reactions to identify the "viral" proteins from within a crude mixture of other proteins which are said not to be "viral" proteins based on the non-specific measurement of the theoretical antibodies. It is mentioned that the there were other stained bands present during gel electrophoresis and that these are artifacts sometimes observed, even in the absence of protein, with this staining procedure. No proper controls were outlined and the only image was of the bands from the gel electrophoresis experiments:

Envelope proteins of avian infectious bronchitis virus: Purification and biological properties

Virus 
The Massachusetts M41 strain of IBV was grown in the allantoic cavities of 11-day-old embryonated chicken eggs and purified on isopycnic sucrose gradients as described by Cavanagh (1981).

Preparation of material for affinity chromatography 
Purified virus was pelleted in a 6 X 14 ml rotor at 70,000 X g for 3 h at 4°C and resuspended phosphate-buffered saline (PBS). An equal volume of PBS containing 4% (wt./vol.) NP40 was added, mixed using a Dounce homogeniser and incubated for 2 h at 25°C. The material was centrifuged for 5 min in an Eppendorf microcentrifuge and the resulting supernatant, containing soluble viral components, was used for the affinity chromatography purification. 

Immunoadsorbent preparation 
Monoclonal antibodies (designated A38 and C24) to the spike and membrane proteins respectively of IBV strain M41 were prepared (Mockett et al., 1984). The 
gammaglobulin fraction of ascitic fluids containing either anti-spike or anti-membrane monoclonal antibodies was isolated by salt precipitation using a final concentration of 18% (wt./vol.) Na2SO4. For the spike immunoadsorbent 5.6 mg of gammaglobulin was coupled to 0.75 mg of CNBr-Sepharose 4B (Pharmacia) according to the manufacturers' instructions and for the membranc immunoadsorbent 5.5 mg was coupled to the same amount of gel. Unreactive groups on the gel were blocked using 1 M ethanolamine, pit 8.0, and any non-covalently bound proteins were removed by repeated washings with 0.1 M NaHCO~ buffer, pH 8.3, containing0.5 M NaCI and 0.1 M acetic acid buffer, pH 4.4, containing 0.5 M NaCI. The immunoadsorbent was stored in PBS containing 0.2% NaN3 at 4°C until used. It was washed twice with 3 M NH4SCN in PBS containing 0.1% octylglucoside, four times with PBS and twice with PBS containing 2% NP40 before use. All wash volumes were 10 ml. 

Affinity chromatography 
The solubilised virus preparation was mixed with the immunoadsorbent for 16 h at 4°C using a rotary stirrer. The gel was poured into a chromatography column and washed with PBS containing 0.1% NP40 (40 ml) and PBS containing 0.1% octylglucoside (10 ml). 3 M NH,SCN in PBS containing 0.1% octylglucoside was added and 10 fractions of 1 ml collected. The absorbance at 280 nm of each of the fractions was read using a SP1800 PyeUnicam spectrophotometer. The fractions in the absorbance peak were dialysed against PBS. A sample of each fraction was then subjected to electrophoresis in a polyacrylamide gel. Those fractions containing detectable viral protein were pooled and constituted the purified protein preparation."

"The viral proteins purified by affinity chromatography are shown in Fig. 1. The spike protein, which is composed of two polypeptides, was the only protein detected in the two fractions shown using the sensitive silver staining procedure. Similarly the membrane protein was not contaminated with other proteins, although this protein did not stain as well as the spike. There were other stained bands present, but these are artifacts sometimes observed, even in the absence of protein, with this staining procedure."

This paper describes the application of affinity chromatography using monoclonal antibodies for the purification of the two viral structural proteins present at the surface of the IB virion – spike and membrane. A previous report has described procedures for the purification of these viral proteins and also nucleocapsid protein, the only other major structural protein (Cavanagh, 1983). IBV was solubilised in NP40 detergent and centrifuged in a sucrose gradient containing this detergent in order to purify the nucleocapsid protein. The addition of 1 M NaCI to the sucrose solutions was required for the purification of the spike and membrane proteins, as they co-migrated in gradients containing low salt concentrations. However, the nucleocapsid protein could not be purified in gradients containing high salt concentrations. The yield of material from these gradients was relatively low, due to the limited number of fractions which contained purified viral components. In other studies (Cavanagh, 1984) purified spike material contained some nucleocapsid protein and the membrane preparation contained other proteins which were thought to be of cellular origin.

There are a number of advantages in using affinity chromatography. By making use of the specificity of the antibody pure material can be isolated, even from a crude mixture of proteins. The method is very quick and easy and the immunoadsorbent can be used several times. Thus, relatively large amounts of purificd material can be obtained. The availability of spike and membrane proteins in a highly purified form will allow more biochemical, structural and immunological studies to be done."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119818/#__ffn_sectitle

1990

In this first of two studies from 1990, affinity chromatography is once again used to attempt "purification" from cell culture supernatant. This time the cells used were in the form of DBT which are mouse brain tumor cells said to be transformed by Rous Sarcoma "virus." The MHV "virus" was passaged four times and was produced in medium containing fetal calf serum which, again, is a source of many host/cellular components itself. Various other chemical additives were used throughout the processes and in the end, it was admitted that "non-viral" host material was reproducibly present in the samples. No EM images of the purified/isolated spike proteins were shown beyond gel electrophoresis stains:

Protection of Mice from Lethal Coronavirus MHV-A59 Infection by Monoclonal Affinity-Purified Spike Glycoprotein

"Cells and virus 
The A59 strain of MHV (MHV-A59), obtained from the American Type Culture Collection (Rockville, MD, U.S.A.), was plaque-purified twice and passaged four times at a multiplicity of infection (MOl) ofO.Ol on DBT cells.

Antigen preparation 
Virus was produced as described previously in culture medium containing 1 % (v/v) FCS. DBT cell monolayers were infected with MHV-AS9 at an MOl of 0.01 and  medium was harvested 16 hrs post-infection. Cell debris were pelleted and virus concentrated by precipitation with 10% (w/v) polyethyleneglycol in O.S M NaCl. Viral antigens were resuspended and dialyzed against TMEN buffer (0.1 M Tris-acid-maleate, pH 6.2, 0.1 M NaC!, 1 mM EDTA), and kept at -70°C until used. In some experiments, virus was labeled by adding 4 mCi of [3SS]methionine (ICN Biochemicals Canada, Ville St-Laurent, PQ, Canada) to culture medium at 6 hrs post-infection. 

Affinity chromatography 
The E2/S-immunoadsorbent was prepared by coupling five milligrams of purified MAb 7-10A 11 to 1 g of CNBr-activated Sepharose 4B (Pharmacia, Dorval, PQ, Canada), all steps performed according to manufacturer's instructions. For affinity chromatography, concentrated virus was solubilized with 2% (v/v) Nonidet P-40 (NP-40) for 2 hrs at room temperature (RT), and soluble proteins were mixed with the 7-lOA-Sepharose gel and incubated end-over-end for 16 hrs at 4°C. The gel specificity was determined by immunoadsorption of radiolabeled antigen, extensive washing with 0.1 % (v/v) NP-40 (in 0.2 M phosphate buffer, pH 6.2, 0.1 M NaC!, 1mM EDTA), and elution of adsorbed proteins into electrophoresis sample buffer. Otherwise, the gel was poured into a column and washed until the absorbance at 280 nm had dropped to baseline level, after which the column was washed with 4 gel volumes of the same buffer containing 0.1 % (w/v) of octylglucoside for detergent replacement. Elution was carried out by adding 3 M ammonium isothiocyanate to the latter solution. Fractions of 1 ml were collected and dialyzed against O.O5 M ammonium bicarbonate, pH 7.4. A sample of each fraction was lyophilized, resuspended in electrophoresis sample buffer, and analyzed on a 7-1S% linear polyacrylamide gel, prior to fluorography with Enlightning® (Dupont Canada, Lachine, PQ, Canada) for radiolabeled antigen or silver stainingl2. Fractions containing purified E2/S were pooled and used for immunological studies."

Purification and immunogenicity of E2/S glycoprotein
The E2/S glycoprotein used for immunogenicity studies was purified from viral antigens concentrated from 1.8 liters of culture medium from MHV -A59-infected DBT cells. Fractions eluted after immunoaffinity chromatography were analyzed by SDS-PAOE and silver staining. Figure 2 shows that the dimeric and monomeric forms of E2/S were purified without detectable contamination from other viral proteins. However, a contaminant (30 kDa), which was probably of cellular origin, was reproducibly observed. The purified glycoprotein was partially denaturated, as confirmed by its loss of reactivity with the MAb 7-10A (data not shown)."

https://link.springer.com/chapter/10.1007/978-1-4684-5823-7_28

This second study from 1990 is mostly a serolgical study which also used cell culturing techniques to aquire the "virus" being studied. HEV was said to be "isolated" by nasal swab from a pig where it was grown in MDCK I cells from a dog and "purified" by centrifugation through a sucrose gradient. Keep in mind that sucrose gradient centrifugation, even though it is considered the "gold standard," can not completely purify/isolate particles of the same size, shape, and density. There were no EM images of the spike proteins beyond the gel electrophoresis ink blots presented below. The proteins were claimed to be detected serologically based on stains. The methods used to obtain the results were also poorly defined with no apparent controls:

Isolation and characterization of the acetylesterase of hemagglutinating encephalomyelitis virus (HEV).

"HEV is related to BCV both serologically and in its 
hemagglutinating properties. We analyzed whether HEV also has acetylesterase activity like BCV strain NT-9 of HEV, which has been isolated by nasal swab from a pig (Heb and Bachmann, 1978), was grown in MDCK I cells and purified by centrifugation through a sucrose gradient. The purified virus was analyzed for its ability to release acetate from p-nitrophenylacetate (PNPA)."

"Purified HEV was incubated with 3H- DFP for 30 min at 4°C and then analyzed by SDS-polyacrylamide gel electrophoresis. The result is shown in Fig. 2. Following staining with Coomassie Brilliant Blue the viral proteins N, M, S, and HE became visible. The radioactive label was found to comigrate only with the latter glycoprotein. The identity of the 3H-DFP-labeled protein was confirmed by analyzing the sample in the absence and presence of reducing agents. Under non-reducing conditions the labeled protein was detected in a position expected for a protein with a molecular weight of about 140 kDal. In the presence of dithiotreitol the apparent size is reduced to about 65 kDal indicating that in the native protein monomers are connected by disulfide bonds to form a dimeric
structure. This migration behavior is characteristic for the viral protein involved in the hemagglutinating activity of HEV (Callebaut and Pensaert, 1980) and therefore, in analogy to BCV, is designated HE.

In order to isolate the esterase of HEV from the viral membrane, purified virions were treated with 1% octylglucoside (OG). The nucleocapsid as well as the M-protein were pelleted by centrifugation for 30 min at 25.000 x g (not shown). The glycoproteins remaining in the supernatant (S and HE) were loaded onto a 10-30% sucrose gradient in PBS containing 1% OG. Following centrifugation at 42.000 rpm for 16 h in SW55 rotor, fractions were collected from the bottom of the tube and analyzed by SDS-polyacrylamide gel electrophoresis. As shown in Fig. 3, S-protein was detected in fraction 3, while most of HE was recovered from fraction 6. Analysis of the fractions for acetylesterase activity revealed that only fractions containing HE were able to release acetate from PNPA. This result confirms that HE is responsible for the esterase
activity of HEV."

https://link.springer.com/chapter/10.1007/978-1-4684-5823-7_16

1991

In this last study, BCV was grown in MDCK I cells, a subline of
Madin-Darby canine kidney cells. Once again, ultracentrifugation was used to "purify" the already contaminated and impure concoction with the addition of phosphate buffered saline and other chemicals such as n-octylglucopyranoside, a nonionic detergent used for membrane protein solubilization. The researchers then used EM images to determine that the S protein, designated as the long projection arm of the "virus," must be reasonably assumed to be used by the "virus" to attach to cells in order to hijack them as it will encounter the cell first…as it is longer.

The S Protein of Bovine Coronavirus Is a Hemagglutinin
Recognizing 9-0-Acetylated Sialic Acid as a Receptor Determinant

"Viruses and cells. Strain L-9 of BCV was obtained from R.Rott (Giessen, Germany). MDCK I cells, a subline of Madin-Darby canine kidney cells, were maintained as described previously (6).

Growth and purification of virus. BCV was grown in MDCK I cells as reported recently (20). Virus was harvested from the supernatant of infected MDCK I cells 48 h postinfection. After clarification of the medium by low-speed centrifugation (2,000 x g, 10 min), virus was sedimented by ultracentrifugation at 112,000 x g for 1 h. The pellet was resuspended in phosphate-buffered saline (PBS) and layered on a sucrose gradient (5 to 50% [wt/wt] in PBS). After centrifugation at 148,000 x g for 40 min, the virus band was collected, diluted with PBS, and sedimented under the same centrifugation conditions. The virus pellet was resuspended in PBS and used for purification of the viral glycoproteins.

Isolation and purification of viral glycoproteins. Viral glycoproteins were isolated by treatment with n-octylglucopyranoside and purified by sucrose-gradient centrifugation as described recently (21)."

"Because of the efficiency of S
protein in recognizing Neu5,9Ac2-containing receptors, it is reasonable to assume that the primary attachment of these coronaviruses is mediated by S protein rather than by HE. This conclusion is in accord with the electron microscopic observation of the viral glycoproteins. They are visible as a double fringe of projections on the virion surface (4). HE protein, which is smaller in size, forms the inner layer of projections. The peplomers, which are characteristic of coronaviruses, form the outer layer of spikes and are made up of S protein. Thus, whenever a virus particle approaches a cell, the cellular receptors will first encounter S protein. For coronaviruses that lack an HE protein, such as avian infectious bronchitis virus, it has been shown that S is the attachment protein (1). From the results presented here, we propose that attachment of all coronaviruses to cell surfaces is mediated by S protein irrespective of the type of receptors recognized."

Ah, another "rosette" conveniently shaped like a "coronavirus."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC250319/

In Summary:
  • Evidence on vaccine effectiveness (VE) against symptomatic illness and severe disease is expected to become available only when variant-updated vaccines have been introduced into broader use
  • In other words, they won't know how well their vaccine works until enough of the fearful and gullible roll up their sleeves and take the plunge…SCIENCE!!!
  • Since the first mRNA vaccines, there has been continuous and substantial "SARS CoV-2 viral" evolution, particularly in the spike (S) protein
  • These genomic changes in the "virus" have resulted in several VOC that have circulated in waves, with varying degrees of immune evasion, some of which have resulted in lower VE of existing "COVID-19" vaccines compared to the initial VE against the index "virus"
  • The magnitude of the reduction in vaccine effectiveness varies by:
    1. Product
    2. Schedule
    3. Disease outcome
    4. Variant of concern (VOC)
    5. Time since last dose
  • Protection against infection and symptomatic illness due to the Omicron variant is lower than other variants and declines rapidly, even after a third (booster) dose
  • Those at highest risk for severe disease, hospitalization, and death remain:
    1. Older persons
    2. Those with comorbidities and immunocompromising conditions
    3. Other vulnerable populations
  • In other words, the vaccines have changed absolutely nothing as the 99% of the people who were not at risk are still not and those who were at risk of disease remain so
  • According to the CDC, mRNA vaccines use mRNA created in a laboratory to teach our cells (because the body is apparently stupid) how to make a protein—or even just a piece of a protein—that triggers an immune response inside our bodies
  • That immune response, which produces antibodies, is what helps protect us from getting sick from that germ in the future (except that it doesn't and people still get sick after "infection")
  • The process is outlined as such:
    1. After vaccination, the mRNA will enter the muscle cells and once inside, they use the cells' machinery to produce a harmless piece of what is called the spike protein
    2. After the protein piece is made, our cells break down the mRNA and remove it (which is assumed but never observed)
    3. Next, our cells display the spike protein piece on their surface and our immune system recognizes that the protein does not belong there
    4. At the end of the process, our bodies have learned how to help protect against future infection with the "virus that causes COVID-19" (except that it doesn't as vaccinated people are continually "re-infected")
    5. Any side effects from getting the vaccine are normal signs the body is building protection (i.e. side effects are a normal sign that the body has been poisoned and is working to rid itself of the poison)
  • "Coronaviruses" are frequently claimed to have a characteristic morphology, including the possession of a "club-shaped" surface projection or spike (S) glycoprotein
  • However, in common with other aspects of the "coronaviruses," the group exhibits variation with respect to the shape, size, and distribution of the S protein on the "virion" surface
  • Dimensions of S vary not only among the "coronaviruses" but also depending on the staining procedure
  • Purification of the S protein of MHV, IBV, HCV strain 229E, bovine "coronavirus" (BCV), and porcine hemagglutinating encephalomyelitis "virus" (HEV) was said to be achieved using a combination of nonionic detergent and sucrose gradient centrifugation and by affinity chromatography
  • In the initial spike protein purification/isolation paper from 1980 listed by David Cavanagh, we can see:
    • The reasons for the apparent diversity in the polypeptide patterns of "coronaviruses" are not fully understood
    • Differences in technique and imperfect discrimination of "virion" polypeptides from those of host origin may account for some of the disparities
    • However, even when the same gel systems and conditions are employed in the same laboratory, significant differences in the number and size of 'virion" polypeptides of different "coronavirus" strains have been observed
    • A spontaneously transformed derivative of the BALB/c 3T3 cell line, designated 17 Cl 1, and the L2 derivation of the L929 cell line were grown in Dulbecco medium supplemented with 10% unheated fetal bovine serum, penicillin (100 U/ml), and streptomycin (100 ,ug/ml)
    • The A59. strain of mouse hepatitis "virus" was produced in 17 Cl 1 cells
    • 17 Cl 1 cell monolayers in glass roller bottles were inoculated with A59 "virus" at a multiplicity of 1 to 10 PFU/cell and after an adsorption period of 1 h at 37°C, 50 ml of Eagle minimal essential medium with 10% unheated fetal bovine serum was added to each roller bottle and the cells were incubated at 37°C
    • Released "virus" was usually harvested 24 to 26 h after inoculation, after several cycles of infection, when high yields were obtained and well before significant amounts of cytopathic changes such as cell fusion or lysis had occurred (i.e. they did not look for the required CPE/lysis to identify if any "virus" was present as it was assumed to be in there)
    • The "virus" was precipitated by the addition of 5.0 g of NaCl per 150 ml of clarified supernatant followed by a half volume of 30% polyethylene glycol to give a final concentration of 10% polyethylene glycol and 2.2% NaCl
    • After multiple centrifugation steps using various chemicals, radiolabeled compounds were added to the medium in final concentration of 2 to 4 uCi of L-3H-amino acid mixture, or [5-3H]uridine per ml, 3 uCi of [6-3H]fucose per ml, and 1 to 4 uCi of [35S]methionine per ml
    • "Purified virions" from three or fewer roller bottles were usually pelleted and resuspended in 1 to 2 ml of TMEN 6 buffer at 4°C
    • NP40, kindly provided by Shell, Inc., was added to a final concentration of 0.25 to 1%, and the mixture was shaken vigorously by hand at least 20 times
    • The detergent-treated "virions" were then layered at 4°C over 15 to 50% sucrose gradients in TMEN 6 buffer containing 0.1% NP40 or at 10°C over 30 to 75% sucrose gradients in TMEN 6 buffer containing 0.1% NP40
    • Continuous 20 to 50% gradients of Renografin-76 containing 0.1% NP40 were employed for dissociation of nucleocapsid complexes
    • For gel electrophoresis used to separate the proteins, each well was loaded with approximately 40 ul of a radiolabeled sample which had been heated to 37°C for 15 min with an equal volume of sample treatment mixture composed of 6 M urea, 4% SDS, 0.05% bromophenol blue in 0.0625 M Tris-chloride, pH 6.7
    • Gels were run at 125 V for about 4 h under constant voltage from a Savant power supply
    • Gels were impregnated with PPO (2,5-diphenyloxazole; Sigma) in dimethyl sulfoxide by the method of Bonner and Laskey, dried with a Savant gel drier onto Whatman no. 17 chromatography paper, exposed to Kodak XR-5 film at -70°C for 1 to 4 weeks, and developed with Kodak X-ray chemicals
    • "Purified, concentrated A59 virus" was disrupted with 1% NP40 and frozen at -75°C in aliquots
    • A 0.1-ml amount of the "virus" preparation was inoculated with complete Freund adjuvant into rabbit footpads, followed after 2 weeks with a second footpad injection of an additional 0.1 ml with incomplete Freund adjuvant (Difco) and 1 week later by an intravenous injection of another 0.4 ml of detergent-treated "virus"
    • "There are two types of Freund's adjuvant: complete and incomplete. Complete Freund's Adjuvant, or CFA, is a water in oil emulsion, which also contains inactivated mycobacteria (Mycobacterium tuberculosis is most frequently used). Incomplete Freund's Adjuvant, or IFA, is the same water in oil emulsion, but does not contain the mycobacteria pathogen." https://prosci-services.com/antibody-development-guide/freunds-adjuvant/
    • After the third injection, rabbits were bled from the ear at 1-week intervals for 1 month
    • For immunoprecipitates of radiolabeled "viral" polypeptides, a 25-ul amount of rabbit serum was incubated with 25 to 200 ul of radiolabeled sample in phosphate-buffered saline containing 0.1% NP40 at 0°C for 1 h
    • Antigen-antibody complexes and antibody were precipitated with an excess of purified, Formalin-fixed staphylococci (Cowan 1 strain) for 10 min at 4°C, pelleted at 3,000 rpm for 10 min, washed three times in 1 ml of 0.05% NP40 with phosphate-buffered saline and then solubilized in sample treatment mixture by boiling for 1 min or treatment at 37°C for 15-30 min
  • Do not feel bad if much of the previous outline went over your head as it is shared in order to show the numerous procedures, manipulations, and alterations the sample must go through to get the desired result
  • In the 1981 purification study, the "virus" once again was a creation from the cell culture process:
    • MHV3 was grown in confluent secondary mouse embryonic fibroblasts
    • Monolayers were infected at an input multiplicity of 0.1 infectious particles per cell and  following an adsorption period of 1.5 hours at 37 ° C, were incubated for 72 hours at 37 ° C in Eagle's MEM with 2 percent foetal calf serum
    • Aliquots of this "virus" suspension were stored at –70°C and used for the preparation of "purified virus" particles and subcomponents
    • The "virus" was pelleted at 75,000 × g for 1 hour and then resuspended in 1 ml Dulbecco's phosphate buffered saline "A" (PBSA)
  • In the 1983 study, the "virus" is another cell-cultured creation:
    • The "virus" was grown in the chorioallantoic membrane (CAM) cells of de-embryonated chicken eggs
    • It is stated that there is less agreement on the composition of the S protein
    • The presumptive S polypeptides of all "coronaviruses" examined were said to have mol. wt. greater than that of the N polypeptide
    • Radiolabelled IBV-M41 was prepared in pairs of de-embryonated eggs; each egg received 125 uCi [35S]methionine (sp. act. > 800 Ci/mmol) or [35S]methionine plus 165 uCi of a mixture of 15 3H-labelled amino acids
    • Unlabelled "virus" was grown in batches of 200 11-day-old embryonated eggs which were  inoculated with approx. 3-5 log10 median ciliostatic dose50 of IBV-M41
    • After centrifugation, the pellet was resuspended in NET buffer (100 mM- NaC1, 1 mM-EDTA, 10 mM-Tris-HCl pH 7.4) to a vol. of 20 ml and sonicated at maximum amplitude for 10 s with the 3 mm probe of an MSE ultrasonic disintegrator
    • Unlabelled markers used were phosphorylase b, bovine serum albumin and carbonic anhydrase; some phosphorylase was pre-stained with Drimarine brilliant blue K-BL and the apparent mol. wt. was 110K
    • These studies were said to show that the peplomers of IBV comprise two glycopolypeptides of 90K and 84K in equimolar proportion while the polypeptides of 110K and 75K, variably detected in "virus" preparations, are probably host polypeptides (in other words, they could not separate out the host material)
  • In 1985, a study was done attempting to purify cell cultured "virus" by way of affinity chromatography:
    • The Massachusetts M41 strain of IBV was grown in the allantoic cavities of 11-day-old embryonated chicken eggs and "purified" on isopycnic sucrose gradients as described by Cavanagh (1981)
    • 'Purified virus" was pelleted in a 6 X 14 ml rotor at 70,000 X g for 3 h at 4°C and resuspended iphosphate-buffered saline (PBS)
    • An equal volume of PBS containing 4% (wt./vol.) NP40 was added, mixed using a Dounce homogeniser and incubated for 2 h at 25°C
    • The immunoadsorbent was stored in PBS containing 0.2% NaN3 at 4°C until used
    • It was washed twice with 3 M NH4SCN in PBS containing 0.1% octylglucoside, four times with PBS and twice with PBS containing 2% NP40 before use
    • The solubilised "virus" preparation was mixed with the immunoadsorbent for 16 h at 4°C using a rotary stirrer
    • The gel was poured into a chromatography column and washed with PBS containing 0.1% NP40 (40 ml) and PBS containing 0.1% octylglucoside (10 ml)
    • 3 M NH,SCN in PBS containing 0.1% octylglucoside was added and 10 fractions of 1 ml collected
    • Those fractions from gel electrophoresis containing detectable "viral" protein were pooled and constituted the "purified" protein preparation
    • There were other stained bands present, but these are artifacts sometimes observed, even in the absence of protein, with this staining procedure
    • This paper describes the application of affinity chromatography using monoclonal antibodies for the "purification" of the two "viral" structural proteins present at the surface of the IB "virion" – spike and membrane
    • IBV was solubilised in NP40 detergent and centrifuged in a sucrose gradient containing this detergent in order to "purify" the nucleocapsid protein
    • The addition of 1 M NaCI to the sucrose solutions was required for the "purification" of the spike and membrane proteins, as they co-migrated in gradients containing low salt concentrations
    • However, the nucleocapsid protein could not be purified in gradients containing high salt concentrations
    • In other studies (Cavanagh, 1984) "purified" spike material contained some nucleocapsid protein and the membrane preparation contained other proteins which were thought to be of cellular origin
    • It is stated that there are a number of advantages in using affinity chromatography and that by making use of the specificity of the antibody pure material can be isolated, even from a crude mixture of proteins
    • In other words, they used theoretical entities to stain the proteins and claimed those were the ones they wanted from within a crude mixture of other proteins…i.e. not purified/isolated at all
  • In the first of two studies from 1990, we again get a cell cultured "virus" grown in DBT cells, a mouse brain tumor cells transformed by Rous Sarcoma "virus:"
    • The A59 strain of MHV (MHV-A59), obtained from the American Type Culture Collection, was plaque-purified twice and passaged four times at a multiplicity of infection (MOl) of O.Ol on DBT cells
    • "Virus" was produced as described previously in culture medium containing 1 % (v/v) FCS (fetal calf serum)
    • Cell debris were pelleted and "virus" concentrated by precipitation with 10% (w/v) polyethyleneglycol in O.S M NaCl
    • "Viral" antigens were resuspended and dialyzed against TMEN buffer (0.1 M Tris-acid-maleate, pH 6.2, 0.1 M NaC!, 1 mM EDTA), and kept at -70°C until used
    • In some experiments, "virus" was labeled by adding 4 mCi of [3SS]methionine to culture medium at 6 hrs post-infection
    • For affinity chromatography, concentrated "virus" was solubilized with 2% (v/v) Nonidet P-40 (NP-40) for 2 hrs at room temperature (RT), and soluble proteins were mixed with the 7-lOA-Sepharose gel and incubated end-over-end for 16 hrs at 4°C
    • The gel specificity was determined by immunoadsorption of radiolabeled antigen, extensive washing with 0.1 % (v/v) NP-40 (in 0.2 M phosphate buffer, pH 6.2, 0.1 M NaC!, 1mM EDTA), and elution of adsorbed proteins into electrophoresis sample buffer
    • Fractions containing "purified" E2/S were pooled and used for immunological studies
    • The E2/S glycoprotein used for immunogenicity studies was "purified" from "viral" antigens concentrated from 1.8 liters of culture medium from MHV -A59-infected DBT cells
    • The dimeric and monomeric forms of E2/S were "purified" without detectable contamination from other "viral" proteins, however, a contaminant which was probably of cellular origin, was reproducibly observed
  • In the second study from 1990, the nose swab from a pig was grown in MDCK cells from a dog:
    • "Purified" HEV was incubated with 3H- DFP for 30 min at 4°C and then analyzed by SDS-polyacrylamide gel electrophoresis
    • Following staining with Coomassie Brilliant Blue the "viral" proteins N, M, S, and HE became visible
    • In order to isolate the esterase of HEV from the "viral" membrane, "purified virions" were treated with 1% octylglucoside (OG)
    • The nucleocapsid as well as the M-protein were pelleted by centrifugation for 30 min at 25.000 x g and the glycoproteins remaining in the supernatant (S and HE) were loaded onto a 10-30% sucrose gradient in PBS containing 1% OG
    • Following centrifugation at 42.000 rpm for 16 h in SW55 rotor, fractions were collected from the bottom of the tube and analyzed by SDS-polyacrylamide gel electrophoresis
    • S-protein was said to be detected in fraction 3, while most of HE was recovered from fraction 6
  • In the last study from 1991, BCV was cultured and grown in MDCK I cells, a subline of Madin-Darby canine kidney cells:
    • "Virus" was harvested from the supernatant of infected MDCK I cells 48 h postinfection
    • After clarification of the medium by low-speed centrifugation (2,000 x g, 10 min), "virus" was sedimented by ultracentrifugation at 112,000 x g for 1 h and the pellet was resuspended in phosphate-buffered saline (PBS) and layered on a sucrose gradient (5 to 50% [wt/wt] in PBS)
    • After centrifugation at 148,000 x g for 40 min, the assumed "virus" band was collected, diluted with PBS, and sedimented under the same centrifugation conditions
    • The "virus" pellet was resuspended in PBS and used for purification of the "viral" glycoproteins
    • "Viral" glycoproteins were isolated by treatment with n-octylglucopyranoside and "purified" by sucrose-gradient centrifugation
    • The researchers state that because of the efficiency of S protein in recognizing Neu5,9Ac2-containing receptors, it is reasonable to assume that the primary attachment of these "coronaviruses" is mediated by S protein rather than by HE
    • This conclusion was in accord with the electron microscopic observation of the "viral" glycoproteins
    • In other words, because the S protein was said to be the longer spikes in the EM images, it can be assumed to be used to attach to cells to infect them
    • Thus, whenever a "virus" particle approaches a cell, the cellular receptors will first encounter S protein
    • From the results presented here, they proposed that the attachment of all "coronaviruses" to cell surfaces is mediated by S protein irrespective of the type of receptors recognized
The smaller the particles get, the more impossible it is to purify and isolate.

How far away removed from reality does a substance need to get before any information gained from it becomes utterly meaningless? In the case of any biological sample, is it the moment the fluid is removed from the living organism in order to be studied in a lab under artificial conditions? Is it the moment that the sample is subjected to unnatural chemicals claimed to keep it alive? Is it when the sample is mixed with foreign genetic materials from other species which it would never come into contact with inside the living organism? Is it when the sample is subjected to unnatural g-forces it would never encounter as it is spun numerous times through ultracentrifugation in order to separate its components? Is it the moment the sample is chemically fixed, dehydrated with ethanol, stained with heavy metals, encased in resin, and blasted with electrons? Or is it the moment the sample is added to a gel and electrocuted for 4 hours until the particles are said to separate? At what point does the biological sample lose itself and become nothing but an illustration in a book?

Concerning the "virus" and its assumed subcomponents including the S protein, the invisible particles are subjected to numerous processes that damage and alter the sample in unmeasurable ways. These include but are not limited to:

  1. The artificial chemicals and conditions encountered during cell culturing the supposed "virus"
  2. The unnatural forces applied to the sample during any purification procedures
  3. The various altercations done during electron microscopy preparation
  4. The high voltages the sample is subjected to during gel electrophoresis

If you do not think that these processes would damage and alter the biological sample with the assumed "virus" beyond recognition to the point that it loses all biological relevance, you obviously do not know how soap is said to destroy "virus" particles and need to take 2 minutes out of your day to watch the short clip below:

Now that you know how hand soap completely destroys the "virus" from this beautifully animated clip, ask yourself how the "virus" and its subcomponents, including the spike protein, supposedly survive the bombardment of added chemicals, compounds, forces, etc. in order to be studied. How do the remnants of particles left after these processes hold any significance to what goes on inside a living organism? How can the assumed "viral" particles within a mixed sample containing foreign genetic material from numerous sources, which are then broken into many smaller intermixed particles of the same size, density, and shape, even be claimed to be coming from the same "viral" source?

It's a 100% guarantee that any living organism would not survive nor remain in the same state it was in if put through similar procedures that these "viral" samples are subjected to. Once you realize this, and once you know that the researchers have admitted numerous times that the current technology not only damages the materials but can also not purify and isolate particles of the same size, shape, and density away from each other, it becomes clear that any information gleaned from these heavily altered and mixed populations hold no significance whatsoever. At best, the particles created serve only as an illustration. A work of twisted art created in a lab. The picture used to sell the story, the fear, and the vaccine. The "coronavirus" and the "spike protein" are just the latest marketing mascots successfully utilized for yet another profitable fear campaign.

stránka nevyužívá cookies, ne špionáž, ne sledování
abychom mohli používat web, zkontrolujeme:
země: CZ · město: Hluboka nad Vltavou · ip: 45.138.104.49
zařízení: computer · prohlížeč: CCBot 2 · platforma:
pult: 1 · online:
created and powered by:
RobiYogi.com - profesionální responzivní webové stránky
00:00
00:00
zavřít
 čekejte prosím načítání dat...