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ViroLIEgy

ViroLIEgy
3 Oct 2022 | 2:43 pm

The Ebola “Virus” Part 2


In part 1 of this breakdown of the fraud that is the Ebola "virus," I looked at the three main publications from three different teams of researchers which were submitted to The Lancet in 1977 as proof for the existence of a new "virus" causing haemorrhagic fever in 1976. The three teams, including one based at the CDC in Atlanta, coordinated with the WHO in order to associate the new "virus" with the non-specific symptoms of disease occuring in Zaire. They did so even though every piece of information aquired through their investigations pointed to the Marburg "virus," which itself was based on the acquisition of fraudulent indirect evidence in 1967.

As the WHO was intimately involved in the coordination of these three teams and the determination of the Ebola "virus" as the causative agent, I thought it would be fun to go through their own recounting of the events that led to this conclusion. In 1978, the WHO was kind enough to release a 23-page report that served as a summary of the information that was aquired during the investigation into the outbreak of haemorrhagic fever in a hospital in Zaire. As the report is rather long, I will provide the relevant highlights. In order to make it easier to breakdown and emphasize the pertinent information, I am doing things a little differently this time around. Instead of presenting the highlights as one continuous text, the provided sections from the report will be broken up by commentary with additional information inserted along the way. There is still the usual summary at the end as well as a link to download the entire report for anyone to read if they so desire. So with that being said, let's jump in and see what we can uncover about this "virus" directly from the WHO:

Ebola haemorrhagic fever in Zaire, 1976

"Between 1 September and 24 October 1976, 318 cases of acute viral haemorrhagic fever occurred in northern Zaire. The outbreak was centred in the Bumba Zone of the Equateur Region and most of the cases were recorded within a radius of 70 km of Yambuku, although a few patients sought medical attention in Bumba, Abumombazi, and the capital
city of Kinshasa, where individual secondary and tertiary cases occurred. There were 280 deaths, and only 38 serologically confirmed survivors.

I want to start by immediately pointing out in this following section, we will see that the common denominator seen in the vast majority of these cases of haemorrhagic fever was the injection of drugs like chloroquine, an anti-malaria drug, at a hospital in Zaire. While I will discuss the use of chloroquine a little later, note that the initial patient was given this injection as he was presumed to have malaria based on his symptoms. After the injection, his symptoms went into clinical remission yet he once again came down with a fever 5 days after his treatment. Spoiler alert: we will later find out that the patient experienced gastrointestinal bleeding after receiving chloroquine and ultimately died on September 8th, 1976:

The index case in this outbreak had onset of symptoms on 1 September 1976, five days after receiving an injection of chloroquine for presumptive malaria at the outpatient clinic at Yambuku Mission Hospital (YMH). He had a clinical remission of his malaria symptoms. Within one week several other persons who had received injections at YMH also suffered from Ebola haemorrhagic fever, and almost all subsequent cases had either received injections at the hospital or had had close contact with another case. Most of these occurred during the first four weeks of the epidemic, after which time the hospital was closed, 11 of the 17 staff members having died of the disease. All ages and both sexes were affected, but women 15-29 years of age had the highest incidence of disease, a phenomenon strongly related to attendance at prenatal and outpatient clinics at the hospital where they received injections. The overall secondary attack rate was about 5%, although it ranged to 20% among close relatives such as spouses, parent or child, and brother or sister.

Note above that pregnant women were among the highest incidence of the symptoms of disease said to be Ebola. Remember this piece of information from the WHO in part 1?

"It can be difficult to clinically distinguish EVD from other infectious diseases such as malaria, typhoid fever and meningitis. Many symptoms of pregnancy and Ebola disease are also quite similar."

https://www.who.int/news-room/fact-sheets/detail/ebola-virus-disease?gclid=Cj0KCQjwj7CZBhDHARIsAPPWv3cNnRDMQ6A8_meGwLE7XzuMOX1WvF97TctCB1A3nu1AfVv0MxnTwi4aAimkEALw_wcB

Hiccups is a symptom of Ebola?!?!

According to the WHO, pregnancy symptoms mimic Ebola. Strangely enough, pregnant women seemingly had the highest incidence of the disease in 1976 and were given injections (presumably of chloroquine but this is not directly stated) in the prenatal and outpatient clinics. What a coincidence!

Active surveillance disclosed that cases occurred in 55 of some 550 villages which were examined house-by-house. The disease was hitherto unknown to the people of the affected region. Intensive search for cases in the area of north-eastern Zaire between the Bumba Zone and the Sudan frontier near Nzara and Maridi failed to detect definite evidence of a link between an epidemic of the disease in that country and the outbreak near Bumba. Nevertheless it was established that people can and do make the trip between Nzara and Bumba in not more than four days: thus it was regarded as quite possible that an infected person had travelled from Sudan to Yambuku and transferred the virus to a needle of the hospital while receiving an injection at the outpatient clinic.

In this next section, the WHO points out that the symptoms of Ebola are non-specific. They tried to add other conditions under the Ebola brand such as hepatitis, pancreatitis, and disseminated intravascular coagulation (a blood clotting condition leading to massive bleeding associated with inflammation, infection, and cancer) yet the lab results were inconlusive:

Both the incubation period, and the duration of the clinical disease averaged about one week. After 3-4 days of non-specific symptoms and signs, patients typically experienced progressively severe sore throat, developed a maculopapular rash, had intractable abdominal pain, and began to bleed from multiple sites, principally the gastrointestinal tract. Although laboratory determinations were limited and not conclusive, it was concluded that pathogenesis of the disease included non-icteric hepatitis and possibly acute pancreatitis as well as disseminated intravascular coagulation.

As I showed in part 1, the particles claimed to be the Ebola "virus" were admitted to be morphologically identical to those associated with the Marburg "virus" yet the WHO and their counterparts at the CDC stated that these "viruses" were immunologically different based on non-specific indirect antibody results. Interestingly, the "virus" was only said to be "isolated" in 8 of 10 cell cultures performed and the particles were only said to be found in the liver samples of three cases:

This syndrome was caused by a virus morphologically similar to Marburg virus, but immunologically distinct. It was named Ebola virus. The agent was isolated from the blood of 8 of 10 suspected cases using Vero cell cultures. Titrations of serial specimens obtained from one patient disclosed persistent viraemia of 10^6.5-10^4.5 infectious units from the third day of illness until death on the eighth day. Ebola virus particles were found in formalin fixed liver specimens from three cases. Survivors of infection were found to have indirect fluorescent antibodies to Ebola virus in titres of 1:64-1:256 within three weeks after onset of disease and these serum titres persisted with only slight decrease for a period of 4 months.

A total of 201 units (200-300 ml each) of plasma containing Ebola virus antibodies in titres of at least 1:64 were obtained and frozen. Two of these units were used to treat a laboratory worker infected with Ebola virus. This person recovered, which suggests that the antibodies may have helped therapeutically.

Note in this next section, the WHO admits that the transmission of the "virus" ended when stopping the injections at the hospital. How odd. 🤔

Virus transmission was interrupted by stopping injections and by isolation of patients in their villages. Use of protective clothing and respirators, strict isolation of patients, and careful disposal of potentially contaminated excreta and fomites will almost certainly prevent future major outbreaks. The virus is probably rarely transmitted by intfectious aerosols, although infection via large droplets remains a possibility.

We also learn that Ebola antibodies were found in five people who were never sick and had no history of contact with any infected individuals. What this ultimately means is that the WHO was strategically setting the stage so that they have the excuse ready for asymptomatic cases of Ebola when the so-called "specific" antibodies are found in people that they are not supposed to be found in:

Only limited ecological investigations were made, since the epidemiology of the outbreak strongly suggested that the virus had been imported into Bumba Zone. Ebola virus was not
recovered from representative samples of bedbugs or of rodents (Rattus rattus and Mastomys spp.) having more or less close contact with humans. Ebola virus antibodies were found, however, in five persons who were not ill and had not had contact with the "infected" villages or the Yambuku hospital during the epidemic. If these findings can be confirmed by an independent method of testing, they would suggest that the virus is in fact endemic to the region and should lead to further effort to uncover a viral reservoir in Zaire."

If we are to believe the findings as presented by the WHO, the Ebola "virus" originated from an infected person traveling from Sudan to Zaire. This unidentified person recieved treatment at the Yambuku hospital by way of a parenteral injection. The same needle was not sterilized and was then reused on another unsuspecting patient, thus resulting in the spread of the disease from patient-to-patient by way of the continuous use of the same unsterlized needles.

In this next section, the WHO plants the seed for the narrative to follow. It is claimed that only 5 syringes and needles were used for every patient throughout the day. While the WHO claims the needles were not sterilized, they state that the needles were rinsed in pans of warm water and/or boiled.

"Five syringes and needles were issued to the nursing staff each morning for use at the outpatient department, the prenatal clinic, and the impatient wards. These syringes and needles were apparently not sterilized between their use on different patients but rinsed in a pan of warm water. At the end of the day they were sometimes boiled. The surgical theatre had its own ample supply of instruments, syringes, and needles, which were kept separately and auto-claved after use.

Contrary to what the WHO says, the use of heat is a common form of sterilization in hospitals:

"Sterilization is the process of killing harmful microorganisms and bacteria on an object by subjecting them to an environment that they can't endure.

Sterilization can be performed via two main routes: heat application and chemical means. 

Heat is the most common form of sterilization and is used in most hospitals and doctors' offices via an autoclave."

https://study.com/academy/lesson/how-to-sterilize-a-needle.html

The WHO also states that the surgery department used syringes and needles that are autoclaved after use. Thus, we are supposed to believe that the hospital in Zaire apparently had different protocols for sterilizing syringes/needles between outpatient, inpatient, and the prenatal ward versus the surgery department. While possible, is it likely? Does it even matter? As we learned earlier, the WHO stated that "viral" transmission stopped as injections at the hospital stopped. They did not say injections using unsterilized needles. What the WHO wants us to believe is that the "virus" transmission stopped due to the "virus" not being transferred by injections using unsterilized needles being passed between the patients. However, as is always the case, there is a much more plausible and likely scenario.

The index patient was injected with chloroquine after being diagnosed with malaria. In fact, his gastrointestinal bleeding did not occur until after the use of chloroquine. This anti-malaria drug is a well-known for its toxic and serious side effects. For a full listing of the reported side effects you can click here but I want to highlight a few of the relevant ones:

  • back, leg, or stomach pains
  • black, tarry stools
  • blood in the urine or stools
  • fever
  • skin rash, hives, or itching
  • sore throat
  • unusual bleeding or bruising
  • upper right abdominal or stomach pain
  • vomiting

Now reread this section from earlier in the WHO's report:

"After 3-4 days of non-specific symptoms and signs, patients typically experienced progressively severe sore throat, developed a maculopapular rash, had intractable abdominal pain, and began to bleed from multiple sites, principally the gastrointestinal tract."

Looks like the symptoms for severe Ebola line up perfectly with the side effects from chloroquine injection. Go figure. 🤷‍♂️

Interestingly, chloroquine has been studied as a drug to treat Ebola patients yet in animals models, it led to worsening of the conditions and death:

"However, while chloroquine inhibited Ebola virus replication in vitro, it caused rapid worsening of Ebola infection in guinea pigs and made no difference to mortality in mice or hamsters."

More about chloroquine and hydroxychloroquine

"When the same dose (90 mg/kg) of chloroquine was given to hamsters challenged with MA EBOV, the study had to be terminated on day 2 after treatment. Nearly all the treated animals, in both the MA EBOV and the mock-challenged groups, died of acute toxicity after administration of chloroquine intraperitoneally, typically within 30 min after treatment (Figure 2, panel B)."

https://wwwnc.cdc.gov/eid/article/21/6/15-0176_article

Thus, we must ask ourselves what makes more sense logically. Was it the "unsterlized" needles spreading a new "virus" or the side effects of injections of toxic drugs which resulted in the symptoms claimed to be Ebola?

Lethal injection.

The following section below details what a probable, possible, and proven case of Ebola is. According to the WHO:

  • Probable: living in endemic area, had received an injection or been around a probable or proven case and died after experiencing 2 or more symptoms
  • Proven: the "virus" was either "isolated" or demonstrated by electron microscopy or they had antibody titres within three weeks of symptoms
  • Possible: a person with a headache or fever with or without other symptoms who had contact with a probable or proven case

Interestingly, the WHO notes that possible cases were treated with antimalarial drugs, antibiotics, and antipyretics to exclude other diseases common to the area. In other words, if they weren't a probable/proven case before treatment, they most likely were afterwards:

"A probable case of Ebola haemorrhagic fever was a person living in the epidemic area who died after one or more days with two or more of the following symptoms and signs: headache, fever, abdominal pain, nausea and/or vomiting, and bleeding. The patient must have, within the three preceding weeks, received an injection or had contact with a probable or a proven case, the illness not having been otherwise diagnosed on clinical grounds. A proven case was a person from whom Ebola virus was isolated or demonstrated by electron microscopy or who had an indirect fluorescent antibody (IFA) titre of at least 1:64 to Ebola virus within three weeks after onset of symptoms. An Ebola virus infection was deemed to have occurred in persons who had a similar IFA antibody titre, but had not been ill during the period 30 August to 15 November 1976.

A possible case was a person with headache and/or fever for at least 24 hours, with or without other signs and symptoms, who had contact with a probable or a proven case within the previous three weeks. These patients were treated with antimalarial drugs, antibiotics, and antipyretics to exclude other diseases common to the area. Persons reporting such symptoms retrospectively were bled and their sera were tested for Ebola virus antibodies. Also any case of fever with bleeding reported to the Ministry of Health from any part of Zaire, whatever the clinical outcome, was regarded as a possible case, and every effort was made to establish a diagnosis by virological or histopathological means."

What is interesting about this next section is how the surveillance teams set out to find cases of the new disease and how they apparently educated the villagers about a disease that they were supposedly still trying to study and understand themselves. The teams were said to have been educated on the differential diagnosis of Ebola from other diseases:

"The objectives of surveillance teams were to find past and active cases of Ebola haemorrhagic fever, to detect possible convalescent cases, to educate the public as to the nature of and means of preventing the disease, and to establish beyond question the termination of the outbreak. Ten special active surveillance teams were recruited and trained. Each consisted of four persons; a team leader (physician or nurse), two nurses, and a chauffeur. The subjects covered during training were the differential diagnosis of Ebola haemorrhagic fever, its epidemiology (including possible modes of transmission), the means of protecting personnel, and methods for obtaining family census data and recording probable and possible cases. The teams were provided with standard forms, a written schedule, and detailed maps showing the villages they were to cover during a two-week period. Each team was assigned a four-wheel-drive vehicle, some of which had radios, and was provided with food, water, gowns, caps, gloves, boots, respirators, and equipment for obtaining blood samples. Chloroquine, tetracycline, aspirin, and a drug against intestinal parasites were all supplied in tablet form. A physician supervised five teams by  frequent field visits and administrative reviews."

According to the Medical Dictionary, differential diagnosis is defined as:

1. A list of conditions that may cause a particular clinical sign or symptom.

2. The arrival at a diagnosis by means of comparing the similarities and differences in various clinical signs.

https://medical-dictionary.thefreedictionary.com/differential+diagnosis

"Many of these diseases present non-specifically, often with fever and malaise. In advanced cases, hemorrhage is common, but may be present in only about 50% of EVD cases. There have been at least 20 suspected cases of EVD in the U.S.; however, only about one-fifth of these cases met criteria for testing. Nevertheless, these suspected cases drain limited healthcare resources because of the heightened concern for EVD. Some of the patients ultimately had malaria and influenza." https://westjem.com/perspective/ebola-virus-disease-essential-public-health-principles-clinicians.html

In order to diagnose a condition, there must be differences in the clinical signs and symptoms. This creates a bit of a problem as the symptoms of Ebola mimic many other more common diseases including influenza, malaria, typhoid fever, meningitis, yellow fever, and even pregnancy. There are no obvious differences in symptomology which is why the CDC and the WHO both state that diagnosis based on symptoms alone is difficult (i.e. impossible) and requires indirect laboratory methods to confirm infection. The CDC states that diagnosis of Ebola requires use of PCR in order to "confirm" a case which was not available to researchers in 1976 as PCR was not invented until 1983. In the WHO's August 2014 Ebola and Marburg virus disease epidemics: preparedness, alert, control, and evaluation, it is stated that cases must be laboratory confirmed, reiterating that it is done either by way of PCR or by non-specific IgM antibody tests:

"LABORATORY-CONFIRMED CASES:
Any suspected or probable cases with a positive laboratory result. Laboratory-confirmed cases must test positive for the virus antigen, either by detection of virus RNA by reverse transcriptase-polymerase chain
reaction (RT-PCR), or by detection of IgM antibodies directed against Marburg or Ebola."

There is absolutely no way any of these teams would have been able to differentially diagnose anyone based on clinical symptoms alone. In fact, the researchers in 1976 had 15 possible cases of haemorrhagic fever that mimicked Ebola:

"Fifteen possible cases of haemorrhagic fever occurring outside the main epidemic area were investigated from Kinshasa. Ebola haemorrhagic fever was ruled out in each instance on clinical, virological, or pathological grounds. Final diagnoses included typhoid fever, viral hepatitis, amoebiasis, acute pulmonary oedema, and carbon monoxide poisoning."

They ultimately decided these 15 cases of haemorrhagic fever were not real cases of Ebola as the results of previously established indirect methods led to diagnoses such as typhoid fever, "viral" hepatitis, amoebiasis, acute pulmonary oedema, and carbon monoxide poisoning. The only method to "diagnose" an Ebola case was either through elimination based on these previously established indirect methods for other diseases associated with the same symptoms or by way of non-specific indirect antibody results. This was the circular way in which they can claim a person experiencing a set of symptoms is an Ebola patient in one case while someone else with the same symptoms is a malaria patient in the other. They love to ignore the fact that, in order for any of these tests to be accurate, not only must the "virus" in question be purified and isolated first in order to calibrate and validate the tests, disease prevalence must also be known first. Disease prevalence can only be determined by clinical diagnosis through differentiating symptoms between these diseases which is an admitted impossibility, thus the case results in 1976 on up to today are utterly meaningless.

Origin and course of the epidemic

As I previously spoiled, we find out here that the initial Ebola patient was diagnosed with malaria, given a chloroquine injection, and had his symptoms subside for a few days only to have them come back worse than before. The patient ultimately died of gastrointestinal bleeding a few days later:

"The first known case, a 44-year-old male instructor at the Mission School, presented himself to the outpatient clinic at Yambuku Mission Hospital (YMH) on 26 August 1976 with a febrile illness thought to be malaria. This man had toured the Mobaye-Bongo zone in the northern Equateur Region by automobile from 10 to 22 August with 6 other Mission workers. The group visited some of the larger towns (Abumombazi, Yakoma, Katokoli, Wapinda) along the road from Yambuku to Badolit, but never arrived at that village because a bridge had been washed away a few kilometres east of the town. On 22 August, fresh and smoked antelope and monkey meat were purchased on the road about 50 km north of Yambuku. The patient and his family ate stewed antelope on his return, but not the monkey meat. He was given chloroquine by parenteral injection on 26 August. His fever resolved rapidly and he was afebrile until 1 September when he again had fever to 39.2° C. Other symptoms and signs ensued and he was admitted to YMH on 5 September with gastrointestinal bleeding. He died on 8 September.

It is also noted that 9 other cases of haemorrhagic fever occurred within the first week and all of them had been treated for other diseases at the hospital. None of the initial diagnoses for these 9 cases were recorded.

At least 9 other cases occurred during the first week of September, all among persons who had received treatment for other diseases at the outpatient clinic at YMH. Names of persons treated at the outpatient clinic and specific diagnoses were not recorded. Thus, it was impossible to determine whether persons with fever had visited YMH in late August. It was of interest, however, that a man about 30 years of age had been admitted to the medical ward on 28 August suffering from "dysentery and epistaxis", a diagnosis not otherwise listed in the preceding eight months. This man, listed as resident in Yandongi, the capital village of the collectivity some 7 km from Yambuku, was taken from the hospital two days later. He turned out to be a person completely unknown to the residents and authorities of Yandongi.

However, it was stated that parenteral injection was the principal mode of administration of nearly all medicines:

Case histories quickly suggested that YMH was a major source of dissemination of Ebola haemorrhagic fever. It was learned that parenteral injection was the principal mode of administration of nearly all medicines."

For those unfamiliar, parenteral injections are given through the skin usually in one of five ways: subcutaneous (into the fat), intraperitoneal (in the stomach), intravenous (in the veins), intradermal (under the skin), and intramuscular (in the muscle). This process bypasses the skin and mucuos membranes leading to some notable drawbacks for this mode of treatment such as:

1. Drug administration by these routes is irreversible and poses more risks than the other routes

2. It is an invasive route of drug administration and thus, it can cause fear, pain, tissue damage, and/or infections.

3. Injections have limitations for the delivery of protein products, particularly those that require sustained levels.

4. It is generally riskier.

5. The preparation to be injected has to be sterile.

6. Drug administered by parenteral routes with the exception of intra-arterial route might still be eliminated by first-pass metabolism in liver prior to distribution to the rest of the body.

7. Help is always needed to administer a parenteral dosage form.

https://www.pharmapproach.com/parenteral-route-of-drug-administration-advantages-and-disadvantages/

This affirms that the medical interventions utilizing risky injections with known toxic side effects were the most likely source of disease, including symptoms such as gastrointestinal bleeding. Of course, in the eyes of the WHO, it couldn't be that the injections of toxic medications were capable of producing said symptoms and were the likely culprit of disease as it had to be a new "virus." However, how they could possibly conclude this after these next admissions is beyond me:

"All ages and both sexes were affected (Table 3) but females slightly predominated. Age/sex attack rates, using the Yandongi collectivity as the population denominator, showed that adult females had the highest attack rate. Much of this excess illness was associated with receipt of parenteral injections at YMH or one of its clinics. The distribution of disease by age group and type of transmission was essentially equal for both sexes except for injection-associated illness among persons 15-29 years old. Females comprised 22 of 24 such cases in the 21-village study.

The single common risk factor in comparison with matched family and village controls for 85 of 288 cases where the means of transmission was determined, was receipt of one or more injections at YMH. Injections received away from YMH were very unusual. Other factors such as previous case-contact, exposure to food, water, hospital buildings, domestic and wild animals, or travel within three months prior to onset, were not associated with this type of transmission. An additional 149 persons acquired the disease following contact with patients, usually in their home villages, and 43 cases had a history of both patient contact and receipt of injection within three weeks prior to onset of illness. Seventeen persons who lived outside Yambuku had contact at YMH and may have received injections there without reporting this fact to their family.

Most of the cases related to injection occurred during the first 4 weeks of the epidemic (Fig. 4). Indeed, it seems likely that closure of YMH was the
single event of greatest importance in the eventual termination of the outbreak.

Several parameters were compared for persons acquiring infection by contact and injection, respectively. Although no statistically significant differences were found in terms of duration of symptoms and signs of illness (Table 4), no person whose contact was exclusively parenteral injection survived the disease."

According to the WHO, the excess illness seen was associated with the injections. The disease in women 15-29 years old was higher for those who had been injected during pregnancy. They called these "injection-associated illnesses." The single common denominator amongst all cases was the receipt of one or more injections of medications capable of producing the symptoms associated with the disease. There were no survivors amongst those who received the injections and after stopping these treatments, the outbreak ended. Even after summarizing these events, the invasive injection and the toxic medications were seemingly not a concern for the WHO. As is always the case, all other much more logical potential causes were pushed aside for the illogical invisible enemy.

"Five consecutive generations of transmission of Ebola haemorrhagic fever were documented in one instance. No sporadic, apparently spontaneous, probable cases were recorded. When "family" was defined as all persons living in contiguous housing and sharing common eating facilities, secondary attack rates never exceeded 8 % (Table 6)."

"In December 1976 and January 1977, sera were solicited from as many people as possible; a total of 236 were obtained. Three persons, 2 of them in clinically noninfected households, who had not had symptoms during or since the epidemic, were found to have Ebola virus IFA titres of at least 1:64. All 3 had experienced contact with fatal cases."

Serological and ecological studies

The test says Ebola "Virus" on it so it must be specific. 😉

In these next few highlights, we find that the antibody measurements, said to be specific and used for diagnosis, are not so specific and were in doubt. The WHO even stated that they were awaiting development of a type-specific method for final interpretation of the antibody results. It is also shown that there were positive antibody reactions found within healthy people who were not recently sick, had no contact with any probable or proven cases, and had no history of visit to the hospital. In other words, the WHO claimed to have found asymptomatic cases of Ebola using antibody tests which they admit produced doubtful results.

"Serum specimens were obtained in November and December 1976 and January 1977 from 984 persons
resident in 48 of the 55 towns and villages reporting probable cases of the disease. These individuals were
classed as clinically ill, not ill but in contact with a case, or neither ill nor in contact. More than half of the subjects were resident in 8 villages, each having more than 5 probable cases. These persons were bled during rapid survey excursions, taking the entire family as the unit of study. The composition of these groups by age, sex, and epidemiological characteristic is given in Table 7 together with the number and category of persons having Ebola virus IFA titres of at least 1:64. Data from Yamolembia I are included. Thirty-eight positives were found. Twenty (16.5%) of 121 ill persons were confirmed as having had Ebola haemorrhagic fever, and 10 (2.5%) of 404 persons in contact with cases also had such antibodies. There were 4 antibody-positive persons who admitted neither illness nor contact with patients. These people were questioned a second time and bled again, and confirmed to have Ebola IFA antibodies. Antibodies were found also in sera of 4 people whose history was not clear and who could not be found a second time for confirmatory study.

In a further effort to document either concurrent asymptomatic infection or possible past infection with Ebola virus, 442 persons were bled in 4 neighbouring villages that had had no fatal cases of the disease. Sera from 5 persons 8-48 years old contained IFA antibodies in titres of 1:64. None of these people were sick, had had contact with persons in other villages, or had visited YMH during the epidemic.

Sera from 58 persons in various exposure categories had anti-Ebola IFA titres of 1:4-1:32. The specificity of these reactions was doubted when it was found that samples from 4 of 200 San Blas Indians from Panama also had such "antibodies" for Ebola but not Marburg virus. Final interpretation of these data awaits development of another method for measurement of type-specific antibodies to these agents."

The asymptomatic infection excuse is still in use today to cover up finding so-called "specific" antibody results in healthy people. From a 2014 Lancet study:

"Evidence suggests that many Ebola infections are asymptomatic, a factor overlooked by recent outbreak summaries and projections. Particularly, results from one post-Ebola outbreak serosurvey showed that 71% of seropositive individuals did not have the disease; another study reported that 46% of asymptomatic close contacts of patients with Ebola were seropositive."

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(14)61839-0/fulltext

Hospitalized patients

Here we find that, in 3 cases of EBV at the Ngaliema Hospital, the patients all presented with similar symptoms in the initial stages including fever, headache, anorexia, vomiting, a rash, haemorrhage, and a severe sore throat. However, after a period of days, the symptoms varied between the three patients. This may just have something to do with the fact that each patient was subjected to different toxic treatment cocktails which are outlined in the section below. Not suprisingly, all three succumbed to their ailments after treatment. It was determined that they all suffered hypovolaemic shock, which is a condition where there is sudden and severe blood loss that leads to the heart being unable to pump enough blood throughout the body, eventually resulting in multiple organ failure. One possible cause of this shock is damage to the stomach. What could possibly lead to such an outcome in these patients? Perhaps trauma to the gastrointestinal organs by way of multiple injections of cocktails of toxic medications known to damage the stomach?:

"Early symptoms and signs in all 3 patients at Ngaliema Hospital included fever, headache, anorexia, and vomiting. A morbilliform rash appeared on the anterior trunk in each of these patients on day 5 or 6, spread to the back and limbs, then faded within 48 hours. Haemorrhage and severe sore throat began between the fourth and seventh days of illness. 

One patient had oral and conjunctival petechiae beginning on day 4, haematemesis and melaena from day 4, gingival bleeding on day 7, and bleeding from injection sites on day 8. Another had melaena only, beginning on the sixth day of illness. The third patient had a single episode of haematemesis on day 7 followed by melaena and ecchymosis on the next day. Progressive glossitis and pharyngitis beginning on day 3 were noted in one patient who developed severe erythema and oedema of the soft palate and pharynx leading to pronounced dysphagia. All three patients were febrile throughout the course of illness, with temperatures frequently above 39°C. Two patients had terminal tachycardia. One patient died on day 7 and two on the eighth day of illness. 

Clinical laboratory tests were done on the first patient, but only a few measurements were carried out on the other two cases to avoid undue exposure of hospital laboratory staff to the virus. Leucocyte counts on the first patient were 7600 and 8900/mm3 on days 5 and 7, respectively. Platelets on days 4, 6, and 7 were 162,000, 150,000 and 150,000/mm3; these were days when frank haemorrhage occurred. During this time, serum SGOT rose from 90 to greater than 200 units/ml and the SGPT increased from 40 to more than 200 units/ml. Serum bilirubin rose from 25.6 tmol/l on day 5 to 59.8 tmol/l on day 7. Partial thromboplastin time (PTT) was 47 seconds on the fifth day. This patient produced only 200 ml of urine on the seventh day and none during the next day when she died. The second patient, on whom no laboratory tests were done, became anuric during the last 2 days of life. 

The third patient had white blood cell counts of 9,400 and 12,300/mm3 on days 7 and 8, respectively. Platelet counts on these days were 253,000 and 205,000/mm3, while P17 values were 45 and 50 seconds, respectively. Fibrin degradation products, measured with a commercial kit (Burroughs-Wellcome) were recorded as 1+ and 2+ on days 7 and 8.

The first case was treated with aspirin, antibiotics, corticosteroids, blood transfusion, and intravenous fluids. The second patient received aspirin, hydrocortisone, immunoglobulin, intravenous fluids, and an experimental drug, moroxydine. Enterovioform was given to control diarrhoea but without success. The third patient was treated for unconfirmed malaria during the first 2 days of illness. When the etiological agent of the epidemic was shown to be a Marburg-like virus, she was given, on day 4, 500 ml of Marburg human plasma obtained from a recovered patient in South Africa. This plasma had an IFA titre of 1:32. In anticipation of disseminated intravascular coagulation (DIC), she was given 16,000 units of heparin on day 6 and 30,000 units daily thereafter. Although anticoagulation was unsatisfactory, as shown by the normal PTT on days 7 and 8, she had less clinical bleeding than the other two patients. On the day prior to death she complained of substernal chest pain and had a tachycardia of 136 with a gallop rhythm. Digitalization slowed this rate only slightly. Marked oedema of the face and upper limbs was present.

Although no autopsies were performed, it appeared clinically that these patients died of hypovolaemic shock. Evidence for DIC was fragmentary, but this syndrome may well have precipitated the bleeding and shock in all cases. Postmortem liver biopsy in the first case revealed marked focal hepatic-cell necrosis with large intracytoplasmic eosinophilic inclusions. Marburg virus-like particles were visualized with an electron microscope (2).

Ebola virus was recovered on day 6 from blood specimens from patient 1 and on days 3 and 6 from patient 2. Quantitative virus assays on blood from the third patient are shown in Table 8. No IFA antibodies against Ebola or Marburg viruses were present.

Retrospective field studies

How they want you to believe the antibody tests are made.

If you needed more reason to doubt antibody results, look no further. In this survey of 231 probable cases, 34 had IFA antibodies. 59% of those with antibodies had symptoms thus leaving 41% of those probable cases asymptomatic. Many others who had direct contact with fatal cases reported having had symptoms but no antibodies whatsoever. In other words, many of those who were sick had no antibodies and nearly half of those who had antibodies were never sick:

Questionnaire forms were completed on 231 probable cases 1 year of age or older, 34 individuals who were found to have Ebola virus IFA antibodies, and 198 controls. The numbers of responses obtained for each symptom and the percentages responding positively in these groups are shown in Table 9. Fever and headache were almost invariably present. The headache often radiated to the cervical spine and was associated with low-back pain radiating into the legs. Sore throat was often reported in association with a sensation of a "ball" in the throat. Chest pain and pleuritis were uncommon. Of persons with antibodies, 59% had one or more symptoms, the most prominent being fever, headache, abdominal pain, and arthralgia. Many more persons who had been in contact with fatal cases reported symptoms but had no Ebola virus antibodies. Illness in antibody-positive individuals was, in general, marked by profound
prostration, weight loss, and a convalescent period of 1-3 weeks."

According to the WHO, a urinary protein test, one not in use as a diagnostic today, was utilized early on in the outbreak to diagnose cases. How many of these patients were misdiagnosed based on a faulty test?

"The only clinical laboratory test done on patients admitted to Yambuku Hospital was urinary protein. This was reported as uniformly positive and was used as a major diagnostic criterion by the nursing sisters early in the epidemic.

The WHO admits that the virological studies, arguably the most important part of the (pseudo)scientific evidence needed to understand a new "virus," were limited. This is apparent as they used small sample sizes where "virus isolation" was only attempted in 10 cases and only 4 liver biopsies were performed:

Virological studies were limited. Ebola virus was isolated in African green monkey kidney cells (Vero) from blood specimens in 8 of 10 cases attempted. These specimens were taken 2-13 days after onset of symptoms. Of interest was the simultaneous detection of virus and IFA Ebola antibodies to a titre of 1:32 in one patient. This man was in the 13th and penultimate day of his illness. Ebola virus particles were also visualized in 3 of 4 postmortem liver biopsies obtained from clinically suspect cases."

The Ebola "virus" was said to have the highest case mortality rate since rabies. Perhaps the toxic cocktails injected into these patients may have helped bring about the high amounts of fatality?:

"No more dramatic or potentially explosive epidemic of a new acute viral disease has occurred in the world in the past 30 years. The case mortality rate of Ebola haemorrhagic fever in Zaire of 88% is the highest on record except for rabies infection. In the circumstances it was not surprising that much desired information was never obtained. Delays in recognition, notification to international health agencies, and specific diagnosis of the disease contributed greatly to this outcome. No better example comes to mind to illustrate the need for national disease surveillance and the prompt solicitation of international assistance, nor of the need for the development of international resources, comprising personnel, equipment, transport, communication, and finance, that can be made available in a very few days to cope with such emergencies. 

Interestingly, both Ebola and rabies have a connection to dangerous injections. In the case of rabies, until the 1980's, the treatment involved a series of shots in the stomach:

"There has been confusion among the general public because of historical fears and the painful
injections of anti-rabies vaccination (nerve tissue vaccine administered over the abdomen) given in the past."

https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.who.int/docs/default-source/searo/india/health-topic-pdf/b5010.pdf%3Fsfvrsn%3D619e77a3_2&ved=2ahUKEwian7aUorb6AhXdkIkEHWPEBOg4ChAWegQIFRAB&usg=AOvVaw2S3jACpOqMEg9qBA6fmZj_

In fact, there could be as many as 21 injections into the abdomen for rabies:

"Several years ago, treatment for rabies included 21 injections into a person's stomach. It was extremely painful and involved a long needle. However, since the early 1980s, there's a much different rabies vaccine to treat humans for rabies exposure."

https://www.oklahoman.com/story/lifestyle/health-fitness/2013/07/14/whats-it-like-to-get-a-rabies-shot/60899910007/

As intraperitoneal injections (in the stomach

cavity) are one of the 5 routes used for parenteral treatment, could these Ebola patients in 1976 have been given the toxic drugs in this manner as was done for rabies until the 1980's? Injections of toxic drugs directly into the stomach would be a possible explanation for an increase in gastrointestinal bleeding. Damage to the stomach by way of trauma is also a risk factor for hypovolaemic shock as suffered by the patients in Ngaliema Hospital. Unfotunately, the WHO does not define the route of parenteral injection so we can only speculate.

These next few sections offer some random pieces of information that poke holes into the WHO's story. First, you will see the WHO admit that laboratory data was virtually non-existent for this outbreak, yet they confirm that the clinical picture resembled the Marburg "virus." They thought that the agents "isolated" in Sudan and Zaire were identical but they had yet to perform the (previously admitted to be doubtful) antibody testing to confirm this. The WHO claimed that viremia (the presence of "virus" in the blood) is a constant feature of the "virus" based on a single study involving the small sample size of just one patient. However, the WHO then stated that no evidence was obtained for persistent "viral" carriage in the Zaire cases of Ebola infection, a phenomenon documented on two occasions for Marburg "virus," but warn that this information is based on a small sample size. It seems very clear that the WHO likes to have their cake and ear it too:

Although laboratory data were virtually non-existent, the clinical picture seen in this outbreak resembled illness produced by the related Marburg virus. If anything, the evolution of Ebola haemorrhagic fever appeared to be more inexorable and less variable than Marburg virus infection. Though far from proven, we suspect that acute defibrination syndrome and pancreatitis were major features of the syndrome and severe liver disease was evident.

In contrast to observations made simultaneously in Sudan, the illness in Zaire had fewer respiratory symptoms, a shorter clinical course, and a higher fatality rate (4). Whether this was due to differences in the virulence of the virus per se or to host and ecological variables such as climate (relative humidity) is not known. At the present time the agents recovered from Sudan and Zaire are thought to be identical, although definitive neutralization tests have not yet been done.

Viraemia appears to be a constant feature of Ebola virus infection in man. The virus persisted in large amounts in the blood in the single, well studied case. The finding of both virus and antibodies in the blood of another agonal case 13 days after onset of symptoms raises the possibility, regarded as unlikely, that antigen-antibody complexes may contribute to the pathology of infection. This and a number of other important virological questions can only be pursued for the moment through studies using monkeys. One of the most pressing is the need for a way to make rapid diagnosis in suspected cases of the disease by searching for cells containing viral antigen. Retrospective specific diagnosis of fatal cases by electron microscopic examination of formalin-fixed liver biopsies appears quite promising and should be attempted in all cases of acute febrile haemorrhagic disease in Africa.

No evidence was obtained for persistent viral carriage in the Zaire cases of Ebola infection, a phenomenon documented on two occasions for Marburg virus (5, 6). But it should be remembered that the number of appropriate, immunosequestered sites sampled was very small. However, semen from one patient infected with a Zaire strain of Ebola virus in the United Kingdom contained virus for more than 2 months after onset of symptoms (3).

In the final highlights, we get the WHO's simplified version of events that reiterates earlier points which should have cast doubt on their conclusions that a new "virus" was the cause of an outbreak of a new disease. First, we get the admittance that the Ebola "virus" had a low rate of secondary person-to-person transmission, meaning it did not easily spread even in cases of close contact with "infected" individuals. They state that the way the new "virus" made it to the hospital will never be known, yet they believed it was brought from the Sudan by man. The way that it was decided that the "virus" spread was through the contaminated needles and syringes used for injections into the sick patients. Once these injections stopped, so too did the outbreak:

The Zaire epidemic had all the attributes of a common source outbreak, together with a fortunately low rate of secondary person-to-person transmission. The means by which the virus was introduced into Yambuku Mission Hospital will probably never be precisely known, but it seems possible that it was brought directly from the Sudan by man. Dissemination of the agent into the villages of the region was principally through contaminated equipment used for parenteral injections. The epidemic waned when the hospital was closed for want of medical staff. That careful disposal of contaminated excreta and fomites, as well as strict barrier nursing using respirators, could break the chain of transmission was demonstrated during the small outbreak in Kinshasa. Still simpler isolation precautions and a change in the cultural customs at funerals appears to have contributed to the dying out of infection in the villages.

Interestingly, the WHO admitted that cases brought about by injection were different and more likely to be fatal than those that they claimed were secondary cases aquired without injections. This obviously makes sense when viewed from the standpoint that the non-specific symptoms of disease were the result of the unnatural injection of various toxic medications directly into the patients and not the effect of a new "virus." Secondary cases were nothing more than looking for similar symptoms in villagers and using fraudulent antibody results to claim the symptoms were caused by the same imaginary "virus:"

Although the data were not always statistically convincing, we had the strong impression that Ebola haemorrhagic fever acquired by injection differed from that due to contact with another case. The mortality was higher. In one study, secondary transmission rates also were higher from index cases that were parenterally induced. It may be that increased virus replication and excretion following parenteral infection accounts for all or most of these differences, but other causes were by no means excluded.

The WHO went on to admit that "neonatal" cases were not definitively elucidated. In other words, they could not explain how the babies aquired the disease from the mother. There was apparently no questioning of the injections of harmful medications into the pregnant women potentially bringing about death and disease in infants. It had to be this magical "virus" somehow passing through the placenta and infecting the unborn child:

The observed "neonatal" cases of the disease were not definitively elucidated. One wishes to know whether Ebola virus can pass through the placenta and infect the fetus, and whether virus is present in human milk and is infectious if ingested.

Once again hammering the final nail in the coffin of the Ebola "virus," the WHO reminded us that better antibody tests were needed in order to interpret the results. While fraudulent antibody results should never carry any weight as evidence, these findings were the only way the researchers could differentiate Ebola from "Marburg" and many other "viruses," thus their questionable "accuracy" speaks volumes. The IFA results were essential to the case that Marburg and Ebola were different "viruses" yet the WHO was unsure if these results were correct. They further add that, like the Marburg "virus," the source of the Ebola "virus" was unknown. This should tell you everything you need to know:

Finally, a better method for measuring Ebola virus antibodies is needed in order to interpret the serological findings reported here. That less than 20% of persons gave a history of acute illness following contact with a fatal case was no surprise. Most of these persons had mild, self-limiting diseases, these being highly endemic in the area. But if the IFA data are correct, at least 2.5% of persons in contact with fatal cases experienced subclinical infection. In addition, the finding of antibodies in a few individuals in the absence of any known contact with Ebola virus during the epidemic raises the possibility that the agent is in fact endemic in the Yambuku area and is occasionally transmitted to man. A definitive answer is essential to further ecological exploration of what is now a very mysterious agent. As in the case of Marburg virus, the source of Ebola virus is completely unknown beyond the simple fact that it is African in origin."

bullwho00439-0113-1Download In Summary:
  • Between September 1st and October 24th, 1976, 318 cases of (assumed) acute "viral" haemorrhagic fever occurred in northern Zaire
  • There were 280 deaths, and only 38 serologically confirmed (i.e. non-specific antibody results) survivors
  • The index case in this outbreak had onset of symptoms on September 1st, 1976, five days after receiving an injection of chloroquine for presumptive malaria at the outpatient clinic at Yambuku Mission Hospital (YMH).
  • He had a clinical remission of his malaria symptoms
  • Within one week several other persons who had received injections at YMH also suffered from Ebola haemorrhagic fever, and almost all subsequent cases had either received injections at the hospital or had had close contact with another case
  • All ages and both sexes were affected, but women 15-29 years of age had the highest incidence of disease, a phenomenon strongly related to attendance at prenatal and outpatient clinics at the hospital where they received injections
  • Intensive search for cases in the area of north-eastern Zaire between the Bumba Zone and the Sudan frontier near Nzara and Maridi failed to detect definite evidence of a link between an epidemic of the disease in that country and the outbreak near Bumba
  • Nevertheless it was established that people can and do make the trip between Nzara and Bumba in not more than four days: thus it was regarded as quite possible that an infected person had travelled from Sudan to Yambuku and transferred the "virus" to a needle of the hospital while receiving an injection at the outpatient clinic
  • In other words, they could not establish any link between two outbreaks but still assumed it was possible for a hypothetical scenario where an unknown "infected" individual carried a new "virus" and made their way to the hospital and unknowingly transmitted the new "virus" by way of the same needle being used with other patients
  • After 3-4 days of non-specific symptoms and signs, patients typically experienced
    progressively severe sore throat, developed a maculopapular rash, had intractable abdominal pain, and began to bleed from multiple sites, principally the gastrointestinal tract
  • Although laboratory determinations were limited and not conclusive, it was concluded that pathogenesis of the disease included non-icteric hepatitis and possibly acute pancreatitis as well as disseminated intravascular coagulation
  • This syndrome was caused by a "virus" morphologically similar to Marburg "virus," but immunologically distinct (i.e. everything was identical besides non-specific antibody results)
  • The agent was "isolated" from the blood of 8 of 10 suspected cases using Vero cell cultures
  • Ebola "virus" particles were found in formalin fixed liver specimens from three cases
  • Survivors of infection were found to have indirect fluorescent antibodies to Ebola "virus"
  • A total of 201 units (200-300 ml each) of plasma containing Ebola "virus" antibodies in titres of at least 1:64 were obtained and frozen and used on an "infected" person who recovered, which suggested to them that the antibodies may have helped therapeutically (and the invisible antibodies may have done absolutely nothing while the person recovered despite their use so it amounts to pointless speculation)
  • "Virus" transmission was interrupted by stopping injections and by isolation of patients in their villages (i.e. the stoppage of injections of chloroquine ended the "viral" spread… 🤔)
  • They somehow decided that the "virus" is probably rarely transmitted by intfectious aerosols, although infection via large droplets remains a possibility (yet more evidenceless and baseless speculation)
  • Ebola "virus" antibodies were found in five persons who were not ill and had not had contact with the "infected" villages or the Yambuku hospital during the epidemic (in other words, the antibodies were either non-specific and/or there are asymptomatic Ebola patients walking around…or the more likely scenario that it is all fraudulent)
  • Five syringes and needles were issued to the nursing staff each morning for use at the outpatient department, the prenatal clinic, and the impatient wards
  • These syringes and needles were apparently not sterilized between their use on different patients but rinsed in a pan of warm water and at the end of the day they were sometimes boiled
  • This led the researchers to conclude it was a "virus" being transmitted from person-to-person due to needle use rather than the contents of the injection
  • On a side note, chloroquine injections, as was given to the patients, are known to cause the exact same symptoms associated with Ebola:
    • back, leg, or stomach pains
    • black, tarry stools
    • blood in the urine or stools
    • fever
    • skin rash, hives, or itching
    • sore throat
    • unusual bleeding or bruising
    • upper right abdominal or stomach pain
    • vomiting
  • A probable case of Ebola haemorrhagic fever was a person living in the epidemic area who died after one or more days with two or more of the following symptoms and signs: headache, fever, abdominal
    pain, nausea and/or vomiting, and bleeding
    • The patient must have, within the three preceding weeks, received an injection or had contact with a probable or a proven case, the illness not having been otherwise diagnosed on clinical grounds
  • A proven case was a person from whom Ebola "virus" was "isolated" or demonstrated by electron microscopy or who had an indirect fluorescent antibody (IFA) titre of at least 1:64 to Ebola "virus" within three weeks after onset of symptoms
    • An Ebola "virus" infection was deemed to have occurred in persons who had a similar IFA antibody titre, but had not been ill during the period August 30th to November 15th, 1976
  • A possible case was a person with headache and/or fever for at least 24 hours, with or without other signs and symptoms, who had contact with a probable or a proven case within the previous three weeks
    • These patients were treated with antimalarial drugs, antibiotics, and antipyretics to exclude other diseases common to the area
  • In other words, as long as you experienced one or two of the non-specific symptoms and either had an injection or been around those who were deemed probable/proven by way of indirect electron microscopy or non-specific antibody results, you were considered an Ebola patient
  • The objectives of surveillance teams were to find past and active cases of Ebola haemorrhagic fever, to detect possible convalescent cases, to educate the public as to the nature of and means of preventing the disease, and to establish beyond question the termination of the outbreak (how did they educate the public on the nature and means of preventing a "virus" they were still supposedly identifying and studying? 🤔)
  • The subjects covered during training were the differential diagnosis of Ebola haemorrhagic fever, its epidemiology (including possible modes of transmission), the means of protecting personnel, and methods for obtaining family census data and recording probable and possible cases (how could they differentially diagnose a disease that mimicked many other diseases sharing the exact same symptoms…and even pregnancy?)
  • Chloroquine, tetracycline, aspirin, and a drug against intestinal parasites were all supplied in tablet form (because if you can't find cases naturally, you might as well create them)
  • Fifteen possible cases of haemorrhagic fever occurring outside the main epidemic area were investigated from Kinshasa and Ebola haemorrhagic fever was ruled out in each instance on clinical, virological, or pathological grounds (i.e. the indirect evidence pointed to other assumed causes)
  • Final diagnoses included:
    • Typhoid fever
    • "Viral" hepatitis
    • Amoebiasis
    • Acute pulmonary oedema
    • Carbon monoxide poisoning
  • The first patient was given chloroquine by parenteral injection on August 26th and his fever resolved rapidly and he was afebrile until 1 September when he again had fever to 39.2° C
  • Other symptoms soon followed and he was admitted to YMH on September 5th with gastrointestinal bleeding and died on September 8th
  • It was learned that parenteral injection (injections into the body by various routes) was the principal mode of administration of nearly all medicines
  • The single common risk factor in comparison with matched family and village controls for 85 of 288 cases where the means of transmission was determined, was receipt of one or more injections at YMH
  • Other factors such as previous case-contact, exposure to food, water, hospital buildings, domestic and wild animals, or travel within three months prior to onset, were not associated with this type of transmission
  • 43 cases had a history of both patient contact and receipt of injection within three weeks prior to onset of illness
  • Seventeen persons who lived outside Yambuku had contact at YMH and may have received injections there without reporting this fact to their family
  • No person whose contact was exclusively parenteral injection survived the disease
  • Indeed, it seems likely that closure of YMH was the
    single event of greatest importance in the eventual termination of the outbreak
  • In other words, the risky and unnatural mode of injection as well as the toxic medications capable of producing the same exact symptoms are all that is needed to explain these cases, not a new invisible "virus"
  • No sporadic, apparently spontaneous, probable cases were recorded
  • When "family" was defined as all persons living in contiguous housing and sharing common eating facilities, secondary attack rates never exceeded 8%
  • Efforts were made to document either concurrent asymptomatic infection or possible past infection with Ebola "virus"
  • Sera from 5 persons 8-48 years old contained IFA antibodies in titres of 1:64 and none of these people were sick, had had contact with persons in other villages, or had visited YMH during the epidemic (i.e. they were asymptomatic)
  • Sera from 58 persons in various exposure categories had anti-Ebola IFA titres of 1:4-1:32 yet the specificity of these reactions was doubted when it
    was found that samples from 4 of 200 San Blas Indians from Panama also had such "antibodies" for Ebola but not Marburg "virus"
  • Final interpretation of these data awaited development of another method for measurement of type-specific antibodies to these agents
  • In other words, the antibody results claimed to be specific were not so specific and the antibody results needed to be confirmed with a yet undeveloped "more specific" method
  • Early symptoms and signs in all 3 patients at Ngaliema Hospital included fever, headache, anorexia, and vomiting yet the remaining symptoms varied amongst them
  • Clinical laboratory tests were done on the first patient, but only a few measurements were carried out on the other two cases to avoid undue exposure of hospital laboratory staff to the "virus"
  • The first patient was treated with aspirin, antibiotics, corticosteroids, blood transfusion, and intravenous fluids
  • The second patient received aspirin, hydrocortisone, immunoglobulin, intravenous fluids, an experimental drug, moroxydin, and enterovioform to control diarrhoea but without success
  • The third patient was treated for unconfirmed malaria during the first 2 days of illness and when the etiological agent of the epidemic was shown to be a Marburg-like "virus," she was given, on day 4, 500 ml of Marburg human plasma obtained from a recovered patient in South Africa
  • All three patients died after treatment
  • Although no autopsies were performed, it appeared clinically that these patients died of hypovolaemic shock (rapid loss of blood that can be caused by internal bleeding in the abdominal organs and digestive tract)
  • Marburg "virus-like" particles were visualized with an electron microscope in one case
  • No IFA antibodies against Ebola or Marburg "viruses" were present in any of the 3 victims
  • Questionnaire forms were completed on 231 probable cases 1 year of age or older, 34 individuals who were found to have Ebola "virus" IFA antibodies, and 198 controls
  • Of persons with antibodies, 59% had one or more symptoms, (41% apparently had no symptoms) the most prominent being fever, headache, abdominal pain, and arthralgia
  • Many more persons who had been in contact with fatal cases reported symptoms but had
    no Ebola "virus" antibodies
  • Here we can see how unreliable antibody results are when 41% had no symptoms of disease and those who had symptoms after contact with fatal cases had no antibodies whatsoever
  • The only clinical laboratory test done on patients admitted to Yambuku Hospital was urinary protein which was reported as uniformly positive and then used as a major diagnostic criterion by the nursing sisters early in the epidemic (note: this is not a diagnostic used today which leads one to wonder how many early cases were misdiagnosed using a faulty method no longer in use?)
  • Virological studies were said to be limited
  • Ebola "virus" was "isolated" in African green monkey kidney cells (Vero) from blood specimens in 8 of 10 cases attempted.
  • Ebola "virus" particles were also visualized in 3 of 4 postmortem liver biopsies obtained from clinically suspect cases
  • The case mortality rate of Ebola haemorrhagic fever in Zaire of 88% is the highest on record except for rabies infection
  • Although laboratory data were virtually non-existent, the clinical picture seen in this outbreak resembled illness produced by the related Marburg "virus"
  • At that time, the agents recovered from Sudan and Zaire were thought to be identical, although definitive neutralization tests had not yet been done
  • Viraemia appeared to be a constant feature of Ebola "virus" infection in man as the "virus" persisted in large amounts in the blood in the single, well studied case (one case 🤣)
  • The WHO stated that a number of other important virological questions can only be pursued for the moment through studies using monkeys
  • No evidence was obtained for persistent "viral" carriage in the Zaire cases of Ebola infection, a phenomenon documented on two occasions for Marburg "virus"
  • The Zaire epidemic had all the attributes of a common source outbreak, together with a fortunately low rate of secondary person-to-person transmission (i.e. not that infectious nor transmissable)
  • According to the WHO, the means by which the "virus" was introduced into Yambuku Mission Hospital will probably never be precisely known, but it seemed possible that it was brought directly from the Sudan by man
  • Dissemination of the agent into the villages of the region was principally through contaminated equipment used for parenteral injections (see how they made it about "contaminated" needles rather than the mode of injection with numerous toxins?)
  • The epidemic waned when
    the hospital was closed for want of medical staff (and thus stopping the injections of toxic drugs)
  • The WHO had the strong impression that Ebola haemorrhagic fever acquired by injection differed from that due to contact with another case as the mortality was higher
  • The observed "neonatal" cases of the disease were not definitively elucidated
  • The WHO again admitted that a better method for measuring Ebola "virus" antibodies was needed in order to interpret the serological findings reported here (which is a pretty troubling admittance when the only way they claimed a new "virus" as well as past and present cases was based on antibody results)
  • That less than 20% of persons gave a history of acute illness following contact with a fatal case was apparently no surprise
  • The WHO stated that if the IFA data are correct, at least 2.5% of persons in contact with fatal cases experienced subclinical infection (those antibody results sure seem rather sketchy based on the WHO's continued hesitancy about their accuracy)
  • In addition, the finding of antibodies in a few individuals in the absence of any known contact with Ebola "virus" during the epidemic raised the possibility that the agent is in fact endemic in the Yambuku area and is occasionally transmitted to man
  • As in the case of Marburg "virus," the source of Ebola "virus" is completely unknown beyond the simple fact that it is African in origin

If we are to believe the findings as presented by the WHO, the Ebola "virus" originated from an infected person traveling from Sudan to Zaire. This unidentified person recieved treatment at the Yambuku hospital by way of a parenteral injection. The same needle was not sterilized and was then reused on another unsuspecting patient, thus resulting in the spread of the non-specific symptoms of disease from patient-to-patient by way of the continuous use of the same unsterlized needles. This may make some sort of sense to those who are still under the "viral" spell and are unwilling to dig a little deeper than just scratching the surface. However, for anyone looking at the evidence presented critically and logically, there is a much more reasonable explanation for the apparent outbreak of disease other than a newly discovered Ebola "virus."

The symptoms associated with the Ebola "virus" are non-specific and mimic other diseases common to the area including influenza, malaria, yellow fever, typhoid, and even pregnancy thus the symptoms were not new or unheard of. The original patient was treated for malaria by way of an injection of chloroquine. While his malaria symptoms were said to clinically disappear after treatment, more severe symptoms showed up days later and the patient eventually succumbed to gastrointestinal bleeding. Chloroquine is a known toxic medication with gastrointestinal problems and unusual bleeding listed as known side effects. The parenteral mode of injection is said to be risky and, if done so through the abdominal cavity, can lead to damage to the organs in the abdomen. Further patients treated at the hospital for unrelated conditions presenting with similar symptoms, including pregnant women, were also given injections of different medications and they too, developed the symptoms associated with severe haemorrhagic fever. Many patients were given cocktails of numerous drugs and antibiotics by way of parenteral injection. Everyone given injections at the hospital eventually died from their illnesses. The WHO even noted that those who received the injections had a different presentation of the disease than cases which were unrelated to the injections with the main difference being higher mortality in those who were treated at the hospital. It was observed that once the injections stopped, the transmission of the disease stopped as well. To anyone looking at this logically, it isn't hard to see the connection between the injection of toxic drugs with the associated symptoms of disease. This does not require a new "virus" as an explanation yet the WHO ignored exploring parenteral injections of chloroquine and other toxic (and at least in one case experimental) drugs as a possibilty in their investigations.

When this knowledge is combined with the fact that the researchers never purified nor isolated any "virus" directly from the blood of any sick patient in Zaire as well as the fact that all of the findings from the cell cultured concoctions they created in the lab pointed to the same indirect evidence associated with the Marburg "virus" discovered less than a decade before, it is simply astonishing that they could conclude there was ever a new "virus" to begin with. The only evidence that the researchers used to claim that the Ebola "virus" was somehow a new "virus" distinct from Marburg were the Indirect Fluorescent Antibody test results which were admitted by the WHO to be less than ideal. In fact, the antibody results were all over the place with many people who never had any contact with an Ebola patient and were never sick in any way testing positive for the antibodies said to be specific to the "virus." Meanwhile, many who had symptoms and direct contact with Ebola patients had no antibodies whatsoever. How could the results of such testing tell the researchers that they had a unique "virus?" When one understands the fraud of antibody research and that these theoretical entities have, like "viruses," never been scientifically proven to exist, it is easy to see how the inaccurate results can be used to claim whatever the researchers want them to say. When one also realizes that the results from the antibody testing directly contradicted the Marburg findings thus showing those results to be fraudulent as well, one will understand that the CDC and the WHO were left with no choice but to try and claim a new "virus" related to Marburg was to blame in order to keep the lie about the "accuracy" of the antibody results intact. 

It is pretty clear that the entire Ebola affair was one giant cover-up for the side effects brought about by toxic drugs injected parenterally. As the symptoms were non-specific and aligned with many other diseases common to the area, it was easy for the researchers to find people suffering similar symptoms in order to claim that they too were also victims of the newly "discovered" pathogenic "virus." This pattern of covering up toxic injections with the findings of a novel "virus" was seen a decade before with the Marburg "virus" associated with Polio vaccination experimentation. They also used this same tactic to cover up poisoning by way of chemicals such as in the case with Polio and DDT/lead arsenate. Once everyone recognizes this pattern, they will be able to see right through the fraud and then we can all start working together to ensure that these tricks are no longer used to fool the gullible into fear and further poisoning by toxic drugs and injections. Together, we can break this sick cycle once and for all.

ViroLIEgy
26 Sep 2022 | 3:12 pm

The Ebola “Virus” Part 1


A comment was recently left on one of my posts that caught my attention:

If you 🤡s are all so confident viruses don't exist, head over to an African country and expose yourself to ebola. Let me know how that works out for you. I'll be waiting. Then again you're all too 🐔 to prove me wrong.

For some reason, there are people out there who seem to believe that in order for one to prove "viruses" do not exist (a proving non-existence logical fallacy), one must either inject themselves with "infected" blood or expose themselves to "infected" individuals. These people feel that dissecting the studies which have been presented as evidence for the existence of these fictional pathogenic entities is just not convincing enough. In this particular instance, I was told to go to Africa and expose myself to an Ebola patient. This person proudly declared "Prove to me I'm wrong by infecting yourself." Of course if I were to become sick after exposing myself to an Ebola patient, that would in no way prove a "virus" was the cause as environmental toxins, stress and fatigue from travel, changes in nutritional and sleeping habits, etc. could all be potential factors leading to dis-ease. If I were not to get sick, these people will fall back on rescue devices such as naturally occuring antibodies or asymptomatic infection as the likely explanation for any lack of dis-ease. It would ultimately be a fruitless exercise.

Unfortunately for those who make illogical demands like the example above, the burden of proof is on the one who makes the positive claim. If one states that a "virus," exists, the onus is on that person to prove the existence of that particular "virus." The best way to do so would be by presenting the foundational studies relating to said "virus." It is interesting to me that these people never look to the scientific literature to try and establish that these "viruses," such as Ebola, were proven to exist in the first place as claimed. However, I understand their frustration in trying to present the original studies as proof as the scientific evidence simply does not exist anywhere within any of these papers.

Regardless, Ebola is one of what I typically see as the three main "viruses" people love to challenge those who critique virology with, the other two being HIV and rabies which I've covered previously. According to their demands, in order to disprove virology, we must overcome the hurdle of the "Big Three" by physically exposing ourselves to sickened patients. Unfortunately, while I would love a safari, dropping everything and flying to Africa in order to expose myself to imaginary "viruses" isn't really a realistic option for me at this moment in time. However, why incur travel expenses when I can just pick apart the pseudoscientific evidence used as proof for the existence of said "virus" (that these people are unwilling to look at and submit themselves) instead?

This breakdown of the Ebola fraud will be presented in two parts. Part one is focused on the "isolation" of the Ebola "virus" by three individual groups of researchers in 1976. I have provided the three papers submitted, one from each group, to see if there is any scientific evidence for an Ebola "virus" contained within them. Did the researchers adhere to the scientific method? Was there any attempt to properly purify and isolate the particles assumed to be the Ebola "virus" directly from the fluids of a sick host? Were these purified particles used to expose a susceptible host in a natural way? Were the electron microscope images only of the assumed "viral" particles and nothing else? Did the researchers carry out the proper control experiments? We shall find out.

The second part explores the inconsistencies in the WHO's 23-page report released in 1978 summarizing the research conducted in 1976. There are many different holes within the narrative that require further examination. It will also look at other potential causes for the symptoms experienced by the patients that were bizarrely overlooked by the WHO.

What is the Ebola "Virus?"

According to the CDC, the Ebola "virus" was discovered in Zaire in 1976 (after an outbreak of haemorrhagic fever). The "virus" occasionally likes to make appearances from time to time as outbreaks in Africa. It is said to first spread to humans through contact with an infected animal. After that, the "virus" transfers human-to-human by way of contact with an infected person's bodily fluids:

"Ebola virus was first discovered in 1976 near the Ebola River in what is now the Democratic Republic of Congo. Since then, the virus has been infecting people from time to time, leading to outbreaks in several African countries. Scientists do not know where Ebola virus comes from. Based on similar viruses, they believe EVD is animal-borne, with bats or nonhuman primates being the most likely source. Infected animals carrying the virus can transmit it to other animals, like apes, monkeys, duikers and humans.

The virus first spreads to people through direct contact with the blood, body fluids and tissues of animals. Ebola virus then spreads to other people through direct contact with body fluids of a person who is sick with or has died from EVD. This can occur when a person touches these infected body fluids or objects that are contaminated with them. The virus then gets into the body through broken skin or mucous membranes in the eyes, nose, or mouth. People can get the virus through sexual contact with someone who is sick with or has recovered from EVD. The virus can persist in certain body fluids, like semen, after recovery from the illness."

https://www.cdc.gov/vhf/ebola/about.html

Is the image of the guy dropping a deuce on the floor really necessary WHO?

According to the WHO, we find that this "rare but severe, often fatal illness" can only be spread by those who are symptomatic. The Ebola "virus" is associated with a list of non-specific symptoms, and is often confused in diagnosis with many other diseases and even pregnancy(!):

Symptoms

The incubation period, that is, the time interval from infection with the virus to onset of symptoms, is from 2 to 21 days. A person infected with Ebola cannot spread the disease until they develop symptoms. 

Symptoms of EVD can be sudden and include:

  • Fever
  • Fatigue
  • Muscle pain
  • Headache
  • Sore throat

This is followed by:

  • Vomiting
  • Diarrhoea
  • Rash
  • Symptoms of impaired kidney and liver function
  • In some cases, both internal and external bleeding (for example, oozing from the gums, or blood in the stools).
  • Laboratory findings include low white blood cell and platelet counts and elevated liver enzymes.
Diagnosis

It can be difficult to clinically distinguish EVD from other infectious diseases such as malaria, typhoid fever and meningitis. Many symptoms of pregnancy and Ebola disease are also quite similar. Because of risks to the pregnancy, pregnant women should ideally be tested rapidly if Ebola is suspected.

https://www.who.int/news-room/fact-sheets/detail/ebola-virus-disease?gclid=Cj0KCQjwj7CZBhDHARIsAPPWv3cNnRDMQ6A8_meGwLE7XzuMOX1WvF97TctCB1A3nu1AfVv0MxnTwi4aAimkEALw_wcB

Dr. Piot and the "virus" hunters!

Irregardless of the non-specific symptoms and the similarities of the disease to pregnancy, researchers in 1976, seeing the same signs and symptoms of haemorrhagic fever associated with many conditions, felt for some reason that they had a new "virus" on their hands. To determine that there was a new "viral" outbreak occuring in Zaire, samples from a sick nurse were sent to Dr. Peter Piot in Belgium, a man who had just graduated medical school in 1976 and was training to be a clinical microbiologist. He is credited as one of the researchers who ultimately discovered the new "virus," even though the "virus" he "found" looked exactly like the Marburg "virus," a different "virus" discovered in 1967 which presents with a similar set of symptoms:

The Scientist Who Discovered Ebola

"While working in a lab at the Institute of Tropical Medicine in Antwerp, Belgium, Piot received a cheap plastic thermos containing two vials of blood and some melted ice. Also inside was a handwritten note from a Belgian doctor based in Zaire (presently the Democratic Republic of Congo). The note explained that the blood had been taken from a Belgian nun working in Zaire. She and two hundred others in a remote region of Zaire had become seriously sick with a mysterious illness. The thermos had been flown on a commercial flight from Zaire's capital city in one of the passenger's carry-on bags! Upon opening the thermos, Piot and his colleagues were greeted with a slushy mix of melted ice and blood. Of the two vials only one had remained intact while the other had shattered en route.

Piot and his team suspected the unknown illness to be yellow fever. The Institute of Tropical Medicine was qualified to handle yellow fever. Little did they know that the as yet to be named Ebola virus was lurking inside the thermos. In those days biosafety protocols were not as strict as they are today. Wearing only thin latex gloves, the scientists removed a sample of blood from the undamaged vial and carried out standard tests on it. The blood sample was screened for known microbes, yellow fever, and several hemorrhagic-fever viruses such as Lassa, Marburg, and dengue. None of potential microbes or viruses were found in the blood. Piot also injected mice with samples of the nun's blood. After a weeks time all of the mice were dead.

When the scientists examined the blood under a microscope they were surprised by what they saw. "We saw a gigantic worm like structure- gigantic by viral standards," explains Piot. The only other known virus that was of similar size and shape was Marburg virus. Marburg had first appeared in 1967 when 31 laboratory workers became sick with hemorrhagic fever after coming into contact with infected monkeys. In 1976 only three facilities outside of the Soviet Union were qualified to deal with fatal viruses safely: Porton Down near London, Fort Detrick in Maryland, and what is now the CDC in Atlanta. The World Health Organization ordered the Belgian scientists to send their blood samples to the CDC lab, the world's reference center for hemorrhagic viruses at the time. After analysing the virus, the CDC confirmed that the sample contained a brand new hemorrhagic virus. Dr. Piot says that he experienced a feeling of "incredible excitement" with the discovery of Ebola."

"In retrospect, Dr. Piot says that he was "lucky not to get infected, not only in the laboratory but later on when I was drawing blood from patients and touching them." Following his work with Ebola, Dr. Piot conducted research on the AIDS epidemic in Africa and later became the founding executive director of UNIAIDS, the Joint United Nations Programme on HIV/AIDS. Dr. Piot is currently the Director of the London School of Hygiene and Tropical Medicine."

https://www.nature.com/scitable/blog/viruses101/the_scientist_who_discovered_ebola/

Dr. Piot caught performing the art of sleeping while standing.

Interestingly, while Dr. Piot was widely given credit for discovering the Ebola "virus," there was some controversy surrounding this claim as there were many others said to be involved in the discovery process. Even though Dr. Piot and Co. claimed "isolation" of the identical-to-Marburg-in-every-way "virus," they did not know whether or not it was in fact a new "virus." After insistence by the WHO, researchers at the CDC were sent samples to investigate whether or not Piot's team had found something new:

History credits this man with discovering Ebola on his own. History is wrong

"But Pattyn and his colleagues didn't know what they were looking at. They saw a lasso-shaped virus that resembled Marburg virus — the cause of a similar type of hemorrhagic fever that was discovered nine years earlier — but didn't have the ability to determine for sure whether what they observed was something new.

The Antwerp lab was not equipped to work on deadly viruses like Marburg, so the World Health Organization instructed Pattyn to send the samples to the British military laboratories at Porton Down. Scientists there started studying it, but also sent a sample to the CDC.

The Atlanta team was able to show that the Yambuku outbreak was caused by a previously unknown virus, not Marburg. Webb ran the critical tests.

"Certainly those who should get credit for discovery actually knew they discovered something new," recalled Dr. Joel Breman, a CDC epidemiologist in 1976 who led the field investigation of the outbreak at Yambuku. "Knowing what this is, different from anything else — that is the discovery of a new organism."

The Antwerp, Porton Down, and CDC teams co-published papers describing their roles in the Ebola discovery in the March 12, 1977, issue of the Lancet. There were 15 authors in all."

"In the interview with STAT, Piot acknowledged credit for the actual discovery belongs to Johnson and the CDC team.

He noted, though, that he and others in Pattyn's lab felt they had the right to describe themselves as co-discoverers, because of the work they did to isolate the virus from the original blood sample."

History credits this man with discovering Ebola on his own. History is wrong
Who deserves credit for the ebola "virus" discovery? No one. 🤷‍♂️

Three separate teams made up of 15 researchers were said to be involved in the Ebola "virus" discovery process. There was Dr. Piot's group in Antwerp, the British military group at Porton Down, and the CDC group in Atlanta. It was decided that Piot's group was able to claim that they "isolated" the Marburg-like "virus" while the CDC was given credit as the final say in the determination of the "isolate" as a new "virus" rather than the same ol' Marburg seen in 1967. In spite of the drama involved in properly crediting the discovery of Ebola to the correct individuals, when one examines the three studies submitted to the Lancet in 1977 by all of the researchers involved, one realizes that the question really shouldn't be about who deserves credit for discovering a new "virus" at all. It becomes quite clear upon reading the studies that not a single one of these researchers deserve this recognition as nowhere in any of the papers are particles assumed to be the Ebola "virus" ever properly purified and isolated directly from the fluids of a sick host and then proven pathogenic in a natural way.

For instance, in Dr. Piot's study, what we see is that the blood he received from the ill nurse was never shown to contain any "virus." At no point in time was any purification process (i.e. centrigugation, filtration, precipitation, etc.) ever described anywhere in the paper, thus there is no evidence of assumed "viral" particles being found directly in the fluids of the nurse. All that is described is the usual cell culturing process utilizing Vero cells from African green monkeys, medium 199, and 7.5% calf serum. This is the exact opposite of purification and isolation as many foreign materials and contaminants are not separated but instead added together into a petri dish. The resulting cytopathogenic effect (CPE) observed in the cell cultures was initially determined to be non-specific until the researchers switched the medium at day 5 to one more susceptible to producing CPE and incubated the culture for another week, thus creating the effect that they wanted to see. The pathogenicity studies involved injecting the blood into the brains and stomachs of newborn mice and claiming any deaths were the result of the "virus" rather than the unnatural method of injecting the blood into the animals. Indirect antibody results were non-specific as well and actually triggered for yellow fever, which is what Dr. Piot stated was his initial suspicion. The particles seen under Electron microscopy were not distinct new entities and were actually identical to those associated with the Marburg "virus." No controls were performed using materials from healthy hosts nor those diagnosed with similar symptoms of disease. Upon conclusion, Dr. Piot and Co. stated it was possible that all they had done was "isolate" the Marburg "virus," yet he speculated it may have been a serologically distinct relative or perhaps a new "virus" belonging to the same group of "viruses" as rabies. In other words, they used the same indirect methods and gathered non-specific results and somehow this alerted the WHO that a new "virus" was the cause:

Isolation of Marburg-like Virus From A Case of Haemorrhagic Fever

A 42-year-old woman (patient M.E.) fell ill on Sept. 23, 1976, in Yambuku, Equateur Province, Zaire. She was transported by air on Sept. 25 to Kinshasa, where a haemorrhagic syndrome gradually developed. Clotted blood taken on the 5th day of illness was sent on ice to the Institute of Tropical Medicine, Antwerp. The sample arrived in the evening of Sept. 29 and was kept in the refrigerator.

The next morning serum was inoculated into 6 young adult
mice by intracerebral and intraperitoneal routes, into 2 litters of newborn mice intracerebrally, and into 10 tubes of Vero-cell cultures (grown in medium 199 containing 7.5% calf serum).

The serum was tested by complement fixation for Lassa-virus antibodies (the result was negative) and by neutralisation on Vero cells for antibodies against yellow-fever virus (antibodies were present at 1/30 dilution).

RESULTS OF INOCULATIONS

Mice

One animal was found dead on the 4th day and a second on the 5th day. Brains were taken from these animals and the survivors on the 5th day.

Newborn Mice

On the fifth day of observation one animal was found dead and partially eaten in each litter. In one litter several mice had disappeared on days 6 and 7, leaving only one animal. In the second litter, however, in which the animals had been very healthy during the whole observation period, only three young mice were left: one dead, one paralysed, and one very sick. The brains of these animals were removed and sent to the Microbiological Research Establishment, Porton, for further study.

Vero Cells

During the first 4 days of observation some cells in the bottom of most tubes became detached from the glass surface. Though this was first interpreted as a partial cytopathic effect, it did not increase during the following days and it was then judged to be non-specific. On day 5 the tissue-culture medium was changed to the succinate/succinic-acid buffered medium (as described by Plaisner et al.1) without serum. In our experience this medium permits the observation of Vero cells for several weeks, while many arboviruses produce a cytopathic effect in these conditions. On day 11 a very striking cytopathic effect was observed in these cultures, with most cells still attached to the glass. The cytopathic effect was almost complete on day 12.

ELECTRON-MICROSCOPY FINDINGS

The supernatant fluid of three tubes was decanted and they were filled with 3% glutaraldehyde for 30 min. The cells were then scraped off in a small amount of glutaraldehyde, rinsed with cacodylate-buffered sucrose (7.5%), postfixed in 1% phosphate-buffered osmium tetroxide, and prepared by the albumin coagulation method. Blocking staining was performed with 0.5% uranyl acetate, followed by dehydration and embedding in Spurr's low-viscosity medium. Electron-microscopic examination of ultrathin sections of this material revealed extracellular straight and cross-sectioned virus particles morphologically similar to Marburg virus (fig. 1). Intracellular nucleocapsids were also seen, some of them apparently originating in vesicles (figs. 2 and 3).

At the same time sections of the liver of the patient from whom this virus had been isolated and who had died on Oct. 1 became available. Although the ultra-structure of this tissue was very poorly preserved, similar virus particles were observed.

CONCLUSION

It was concluded that the agent responsible for the epidemic of haemorrhagic fever in Central Africa was either Marburg virus or a virus serologically different from it but belonging to the same virus group, either rhabdovirus or torovirus.

doi: 10.1016/s0140-6736(77)92002-5.

Is that Anthony Fauci?

As the WHO wanted separate investigations of the findings by labs which were better equipped to handle the more dangerous "virus" assumed to have been identified in Antwerp, the Bristish military in Porton Down was called upon to confirm the results. In the Porton Down paper, once again we see an absence of any mention of putifying and isolating the particles assumed to be a "virus." We get the same cell culture experiments using Vero cells as done by Piot's team, even going so far as using material sent from Antwerp. Proton Down acquired from Antwerp the blood of acute-phase patients, the cell culture materials, and the brains from inoculated mice for their own mad science experiments. None of the ingredients used for the culturing process were detailed and even though there is a mention of controls, they remain undefined. During their cell culture experiments, the researchers noted slight cytopathogenic effects which they attributed to the toxic materials used for inoculation. Eventually, three of the cultures changed to a more acidic color and caused illness when injected into the stomachs of young Guinea pigs, thus signaling to the researchers that a "virus" was present. The other pathogenicity studies performed included injecting the brains of mice killed in Antwerp into the brains and stomachs of newborn mice in Proton Down and claiming success when the mice eventually died.

While the researchers assumed that they had a new "virus," the structures seen in EM from the livers in Guinea pigs looked identical to that seen in Guinea pigs and monkeys inoculated during the Marburg "virus" experiments in 1967 and 1975. The cell culture supernatant contained elongated sinuous structures which resembled the structures seen in baby-hamster kidney cells after infection with Marburg "virus." In fact, the researchers admitted that the disease and lesions produced in Guinea pigs by the new agents resembled those in Guinea pigs inoculated with early passage levels of Marburg "virus." For all intents and purposes, the researchers should have, if anything, concluded that they had "isolated" the Marburg "virus." While that conclusion would have been just as fraudulent, at least it would have lined up with what the indirect pseudoscientific evidence pointed towards:

Viral Haemorrhagic Fever in Sounthern Sudan and Northern Zaire

BETWEEN July and September, 1976, sporadic cases of fever with haemorrhagic manifestations were reported in the areas of Nzara, Maridi, and Lirangu in the southern Sudan. The first cases are believed to have been in agricultural settlements. An outbreak of a similar disease was also reported from the zone of Bumba in northern Zaire. As the epidemic increased in intensity, the disturbingly high percentage of cases reported among hospital personnel suggested direct person-to-person spread of infection. The illness began with an acute fever, malaise, sore throat, muscular pains, vomiting, and
diarrhoea. Those severely affected had epistaxis, subconjunctival haemorrhages, haemoptysis, hsematemeses, and melaena. Some patients also had a body rash, tremors, and convulsions.

SOURCES OF SPECIMENS

Specimens from the northern Zaire outbreak were referred to the Microbiological Research Establishment, Porton, by Prof. S. R. Pattyn of the Institute of Tropical Medicine, Antwerp. They were an acute-phase serum (no. 718), cell-culture materials and brains from suckling mice which had already been inoculated with the serum. We later received a specimen of liver from the same patient and also 5 acute-phase blood specimens from Zaire via Professor Pattyn. Specimens from the southern Sudan were mainly collected at Maridi Hospital and sent to us directly by Dr Babiker el Tahir, Dr D. H. Smith, Dr K. Jones, and Dr M. Cornet, who were there to investigate. They consisted of 3 throat swabs, 3 urine specimens, 6 acute-phase blood specimens, and convalescent serum specimens. These specimens were sent on dry ice or in liquid nitrogen. Three laboratories engaged in preliminary studies on the aetiological agent reported the isolation of a virus which
was morphologically similar to Marburg virus.

RESULTS OF ATTEMPTS AT VIRUS ISOLATION

Virus isolation from the original human material was attempted in: (1) culture preparations of Vero cells; (2) suckling mice inoculated intraperitoneally (i.p.) and intracerebrally (i.c.); and (3) young guineapigs (200-250g) inoculated i.p.

Isolation in Guineapigs

So far 5 isolations of the aetiological agent have been obtained in guineapigs: 4 from specimens from northern Zaire and 1 from a specimen from southern Sudan. Guineapigs inoculated with these specimens became febrile 105°F (40-5°C) after an incubation period of 4-7 days. The febrile illness lasted 4-5 days during which the guineapigs failed to thrive and looked ill. 1 of the 12 guineapigs inoculated with original material died on the 12th day after inoculation. The other 11 guineapigs slowly recovered and were subsequently shown to have antibodies detectable by fluorescent antibody tests at titres ranging from 1/64 to 1/128. When whole heparinised blood from febrile guineapigs was inoculated i.p. into other guineapigs it produced a similar febrile illness.

Histopathological Findings

Liver.-There were numerous foci of necrosis which had no consistent lobular distribution and consisted of groups of liver cells undergoing hyaline degeneration and necrosis. In some of the degenerating cells small pleomorphic eosinophilic bodies were present in the cytoplasm which were periodic-acid/Schiff positive and stained bright red with the Machiavello technique but did not stain metachromatically with Giemsa. Kupffer cells were enlarged, some sinusoids contained lymphocytes, and the periportal areas were heavily infiltrated by lymphoreticular cells.
Spleen and lymph-nodes.-There was widespread depletion of the lymphoid tissue of the follicles, which contained small zones of necrosis. Large numbers of macrophages were accumulated in the sinuses.
Lungs.—Changes in the lungs were slight: localised thickening and infiltration of interalveolar septa by lymphoreticular cells.
Other organs.-No lesions were detected in the brain, kidneys, or adrenal glands.

Electron Microscopy of Liver

Small pieces of liver from a guineapig killed 5 days after inoculation were fixed in 1% osmium tetroxide. Ultrathin sections were stained with uranyl acetate and lead citrate and examined under the electron microscope. Fig. 1 shows structures strikingly similar to those seen in the livers of guineapigs and monkeys infected experimentally with Marburg virus.

Isolation in Mice

The brains from suckling mice that became sick after being inoculated with acute-phase serum by Professor Pattyn in Antwerp were reinoculated into four litters of suckling mice. The mice began dying on the Sth day and were all dead by the 9th day. This mouse passage material has not yet been further investigated. We propose to inoculate this material into guineapigs to see whether the characteristic infection develops before we attempt further studies in mice.

Cell-culture Studies

Isolation from the original serum and blood specimens was also attempted in preparations of cultured Vero cells. A partial cytopathic effect was seen under low-power microscopical examination. This effect did not progress to complete destruction of the cell sheet and could be attributed to a toxic effect of the specimens inoculated. There was, however, a distinct colour change in the medium of three of these cultures. By the 6th or 7th day after inoculation they became noticeably more acid than the control cultures. When young guineapigs were inoculated with these three cell cultures a febrile illness developed after 4-6 days.

Electron microscopical examination of the cell-culture fluid revealed elongated sinuous structures (figs 2 and 3) which resembled the structures seen in baby-hamster kidney cells
after infection with Marburg virus.'

CONCLUSIONS

Electron microscopy of infected guineapig livers and cell-culture material revealed structures with a striking resemblance to Marburg virus. The disease and lesions produced in guineapigs by the new agents resemble those in guineapigs inoculated with early passage levels of Marburg virus. Lesions in a liver sample taken at necropsy from one of the Zaire patients were very similar to those produced in the liver of experimentally infected guineapigs. As yet, we have no positive evidence to suggest that the viruses isolated from northern Zaire and southern Sudan are related serologically to the Marburg virus strain isolated in 1967. 18 convalescent sera collected in the Sudan did have fluorescent antibody titres ranging from 1/4 to 1/128 against one of the Zaire virus isolates. Although this evidence is slight it suggests that both outbreaks have been caused by viruses which are related if not identical. Studies are in progress to determine the relationship between the new isolates from Zaire and the Sudan with the Marburg strain isolated in 1967.

doi: 10.1016/s0140-6736(77)92001-3.

Searching hard for that "virus."

The insistence by the WHO for a re-examination of the evidence eventually led to the CDC team in Atlanta also becoming involved in order to have the final say as to whether the "isolates" in Antwerp consisted of a new "virus" or not. In the CDC paper, it is stated that Porton Down sent an aliquot of blood to the CDC. As in the previous studies, this specimen was also inoculated onto Vero cells. Once again, no purification procedures were detailed nor were the exact make-up of the cell culturing materials utilized ever provided. After observing a "distinct" CPE, the unpurified supernatant fluid was used for EM imaging. The researchers stated that they observed large numbers of filamentous particles, which were approximately 100 nm in diameter and varied in length from 300 nm to more than 1500 nm. This is quite a large difference in the size range of the particles which would show that they are not homologous and could potentially have been many different "viruses" and/or microbes. The researchers also noted that, in all details, these particles were indistinguishable from those seen in the previous Marburg "virus" outbreaks. Even liver tissue examination showed the same structures seen in human and Guinea pig livers from the 1967 and 1975 Marburg outbreaks. The only evidence for a proposed difference between what was eventually declared Ebola and the Marburg "virus" were results from indirect immunofluorescence antibody tests which, as the name implies, is a form of INDIRECT evidence using non-specific chemical reactions. In fact, the researchers admit that there was a weak reaction between the Marburg and Zaire samples. However, based on the weak serological evidence (which contradicted previous Marburg findings) and in spite of the numerous admissions to identifying the same particles as associated with the Marburg "virus," the CDC had the final say that the Ebola "virus" was in fact a new "virus." They declared so despite the fact that it is clear that not a single one of the 3 groups of researchers actually purified and isolated an Ebola "virus" to begin with:

Isolation and Characterization of a New Virus Causing Acute Haemorrhagic Fever in Zaire

AN outbreak of haemorrhagic fever with an exceptionally high mortality-rate occurred in southern Sudan and northern Zaire with peak case-rates in September, 1976. A W.H.O. International Commission operated in Sudan and Zaire from October onward. Blood and tissue specimens from persons with haemorrhagic disease were sent to laboratories in Belgium and England, and findings from these laboratories. appear in the accompanying reports. While these specimens were being studied, Mr E. T. W. Bowen (Microbiological Research Establishment, Porton Down) sent an aliquot of an acute blood specimen from a patient in Zaire (no. 718, patient M.E.) to the Center for Disease Control, Atlanta, for additional study.

This specimen, and all subsequent acute specimens, were inoculated into Vero (African green monkey) cells. Three days later a distinct cytopathic change (focal rounding and refractility) was evident, and an aliquot of supernatant fluid was removed for negative contrast
electron microscopy.

ELECTRON MICROSCOPY OF CELL CULTURES

Carbon-coated grids were sequentially floated on droplets of the cell-culture fluid and then on 2% sodium silicotungstate pH 7. Large numbers of filamentous virus particles were seen (fig. 1). They were approximately 100 nm in diameter and varied in length from 300 nm to more than 1500 nm. Many had terminal blebs. Particles had regular surface projections approximately 10 nm long, and when stained they were seen to have internal cross-striations indicative of a helical core structure (fig. 2). In all details, these particles were indistinguishable from Marburg virus particles studied in 1967 (isolates from Germany) and 1975 (isolate from South Africa). Two characteristics were more prominent in the 1976 Zaire isolate: there was more branching of the filamentous particles (fig. 1); and more evidence of envelope continuation beyond the ends of the more rigid internal structure (fig. 1, arrow).

Vero cells infected with the same isolate from Zaire were examined also by thin-section electron microscopy. Filamentous virus particles were found budding from the plasma membrane of cells (fig. 3), and many of the cells contained inclusion bodies. These intracytoplasmic inclusions were complex and distinct, and consisted of a finely fibrillar, or granular ground substance which condensed into tubular structures. The latter have been considered to be the internal helical structure of mature virus particles. These tubules were sectioned randomly, some in cross-section, some linearly. The virus particles in these sections were identical to those observed in the 1967 and 1975 isolates.

POSTMORTEM LIVER SPECIMENS

Evidence of infection was seen by light microscopy in three postmortem human liver specimens from Zaire (received in formalin). Infection of two of these was confirmed by electron microscopy. Focal eosinophilic hepatocellular necrosis with modest inflammatory infiltration was prominent. Large cosinophilic inclusions were present in many intact hepatocytes, especially near sites of severe necrosis (fig. 4). These rather smooth and refractile inclusions were so characteristic that they have diagnostic significance. Plastic-embedded formalin-fixed necropsy specimens were examined with the electron microscope. Although preservation of liver tissue was poor, large numbers of filamentous virus particles and inclusion bodies (masses of tubules) were found (fig. 5) which were indistinguishable from those in Marburg virus-infected human and guineapig livers studied in 1967 and 1975.

ANTIGENIC COMPARISON WITH MARBURG

An antigenic difference between this isolate and Marburg '67 was demonstrated by indirect immunofluorescence (I.F.A.). An infected Vero-cell suspension was placed in drops on slides, air dried, and then acetone-fixed for 10 min at room temperature. Slides were stored at -70°C until tested. Marburg '67 antigen slides, prepared in like manner, were used for comparison. Reciprocal titres obtained with convalescent human sera drawn during the 1967, 1975, and 1976 outbreaks are listed in table I. With the exception of a weak reaction to Marburg antigen at a 1/4 dilution of the Zaire convalescent serum, the new isolate was distinct from Marburg virus. The homologous Marburg titres of 128 and 64 obtained with '67 and '75 antigens and antisera were comparable to those reported by Wulff and Conrad.

A single-injection immune serum to the new agent was prepared in guineapigs, and reciprocal I.F.A. tests were performed with available similar reagents for Marburg virus. Reciprocal titres (table 2) further confirmed the distinctness of the two viruses. Although one of two early convalescent sera from Sudan gave a positive reaction with the Zaire antigen (table I) further work is needed to determine whether the haemorrhagic-disease agents from the two countries are identical.

EBOLA VIRUS

With the concurrence of Prof. S. R. Pattyn, Institute of Tropical Medicine, Antwerp, and Mr E. T. W. Bowen, Microbiological Research Establishment, Porton Down, the name Ebola virus is proposed for this new agent. Ebola is a small river in Zaire which flows westward, north of Yambuku, the village of origin of the patient from whom the first isolate was obtained. In deference to the countries involved and to the lack of specific knowledge of the original natural source of the virus, it is also suggested that no names of countries or specific towns be used.

doi: 10.1016/s0140-6736(77)92000-1

Looking hard or hardly looking?
In Summary:
  • Ebola "virus" was first discovered in 1976 near the Ebola River in what is now the Democratic Republic of Congo
  • Since then, the "virus" has been said to infect people from time to time, leading to outbreaks in several African countries
  • The "virus" first spreads to people through direct contact with the blood, body fluids and tissues of animals
  • Ebola "virus" then spreads to other people through direct contact with body fluids of a person who is sick with or has died from EVD
  • However, a person infected with Ebola cannot spread the disease until they develop symptoms
  • It can be difficult to clinically distinguish EVD from other infectious diseases such as malaria, typhoid fever and meningitis
  • Many symptoms of pregnancy and Ebola disease are also quite similar
  • Regular symptoms include:
    • Fever
    • Fatigue
    • Muscle pain
    • Headache
    • Sore throat
    • Vomiting
    • Diarrhoea
    • Rash
    • Symptoms of impaired kidney and liver function In some cases, both internal and external bleeding (for example, oozing from the gums, or blood in the stools)
    • Laboratory findings include low white blood cell and platelet counts and elevated liver enzymes
  • In 1976, Dr. Peter Piot recieved a thermos containing blood vials with a note which explained that the blood had been taken from a Belgian nun working in Zaire
  • She and two hundred others in a remote region of Zaire had become seriously sick with a mysterious illness
  • Piot and his colleagues were greeted with a slushy mix of melted ice and blood as, of the two vials, only one had remained intact while the other had shattered en route
  • Dr. Peter Piot and his team suspected the unknown illness to be yellow fever
  • Wearing only thin latex gloves, the scientists removed a sample of blood from the undamaged vial and carried out standard tests on it
  • The blood sample was screened for known microbes, yellow fever, and several hemorrhagic-fever "viruses" such as Lassa, Marburg, and dengue
  • None of the potential microbes or "viruses" were found in the blood
  • Under Electron Microscope, Dr. Piot stated: "We saw a gigantic worm like structure-gigantic by viral standards."
  • The only other known "virus" that was of similar size and shape was Marburg "virus"
  • In other words, Piot and Co. found the exact same particles claimed to be Marburg but stated that they did not find Marburg in the blood samples…
  • In retrospect, Dr. Piot said that he was lucky not to get infected, not only in the laboratory but later on when he was drawing blood from patients and touching them
  • Piot and Co. saw a lasso-shaped "virus" that resembled Marburg "virus" — the cause of a similar type of hemorrhagic fever that was discovered nine years earlier — but didn't have the ability to determine for sure whether what they observed was something new
  • Scientists in Porton Down started studying the sample, but also sent a sample to the CDC after insistence by the WHO
  • The CDC's Atlanta team was said to show that the Yambuku outbreak was caused by a previously unknown "virus," not Marburg
  • The Antwerp, Porton Down, and CDC teams co-published papers describing their roles in the Ebola discovery in the March 12, 1977, issue of the Lancet
  • In the interview with STAT, Piot acknowledged credit for the actual discovery belongs to Johnson and the CDC team
  • Serum from the sick nurse was inoculated into 6 young adult mice by intracerebral and intraperitoneal routes, into 2 litters of newborn mice intracerebrally, and into 10 tubes of Vero-cell cultures (grown in medium 199 containing 7.5% calf serum)
  • The serum was tested by complement fixation for "Lassa-virus" antibodies (the result was negative) and by neutralisation on Vero cells for antibodies against yellow-fever "virus" (antibodies were present at 1/30 dilution)
  • During the first 4 days of observation some cells in the bottom of most tubes became detached from the glass surface and although this was first interpreted as a partial cytopathic effect, it did not increase during the following days and it was then judged to be non-specific
  • On day 5 the
    tissue-culture medium was changed to the succinate/succinic-acid buffered medium (as described by Plaisner et al.1) without serum
  • On day 11 a very striking cytopathic effect was observed in these cultures, with most cells still attached to the glass and the cytopathic effect was almost
    complete on day 12
  • In other words, Piot and Co. were not getting the CPE that they wanted to see so the medium was changed to one known to produce CPE with "arboviruses" and by day 12 they got the effect that they wanted to see
  • Electron-microscopic examination of ultrathin sections of this material revealed extracellular straight and cross-sectioned "virus" particles morphologically similar to Marburg "virus"
  • Although the ultra-structure of liver tissue was very poorly preserved, similar "virus" particles were observed
  • It was concluded that the agent responsible for the epidemic of haemorrhagic fever in Central Africa was either Marburg "virus" or a "virus" serologically different from it but belonging to the same "virus" group, either "rhabdovirus" or "torovirus"
  • Specimens from the northern Zaire outbreak were referred to the Microbiological Research Establishment, Porton, by Prof. S. R. Pattyn of the Institute of Tropical Medicine, Antwerp which were an acute-phase serum (no. 718), cell-culture materials and brains from suckling mice which had already been inoculated with the serum
  • Three laboratories engaged in preliminary studies on the aetiological agent reported the isolation of a "virus" which
    was morphologically similar to Marburg "virus"
  • "Virus isolation" from the original human material was attempted in:
    • Culture preparations of Vero cells
    • Suckling mice inoculated intraperitoneally (i.p.) and intracerebrally (i.c.)
    • Young guineapigs (200-250g) inoculated i.p.
  • In inoculated Guinea pigs, a febrile illness lasted 4-5 days during which the Guinea pigs failed to thrive and looked ill
  • 1 of the 12 Guinea pigs inoculated with original material died on the 12th day after inoculation while the other 11 Guinea pigs slowly recovered
  • Small pieces of liver from a Guinea pig killed 5 days after inoculation were fixed in 1% osmium tetroxide and structures strikingly similar to those seen in the livers of Guinea pigs and monkeys infected experimentally with Marburg "virus" were seen
  • The brains from suckling mice that became sick after being inoculated with acute-phase serum by Professor Pattyn in Antwerp were reinoculated into four litters of suckling mice
  • The mice began dying on the 5th day and were all dead by the 9th day yet this mouse passage material had not yet been further investigated
  • In cell culture experiments involving Vero cells, partial cytopathic effect was seen under low-power microscopical examination
  • This effect did not progress to complete destruction of the cell sheet and could be attributed to a toxic effect of the specimens inoculated
  • There was, however, a distinct colour change in the medium of three of these cultures and by the 6th or 7th day after inoculation they became noticeably more acid than the control cultures (which were not defined)
  • Electron microscopy of infected Guinea pig livers and cell-culture material revealed structures with a striking resemblance to Marburg "virus"
  • The disease and lesions
    produced in Guinea pigs by the new agents resemble those in Guinea pigs inoculated with early passage levels of Marburg "virus"
  • The researchers stated that they had no positive evidence to suggest that the "viruses isolated" from northern Zaire and southern Sudan were related serologically to the Marburg "virus" strain isolated in 1967
  • In other words, they had no positive evidence to suggest the "virus," which was identical to Marburg in every other way, was not the exact same "virus" either as they just assumed their new "isolates" were different
  • The researchers admitted that although their evidence was slight, it suggested that both outbreaks were caused by "viruses" which are related if not identical
  • Mr E. T. W. Bowen (Microbiological Research Establishment, Porton Down) sent an aliquot of an acute blood specimen from a patient in Zaire (no. 718, patient M.E.) to the Center for Disease Control, Atlanta, for additional study
  • This specimen, and all subsequent acute specimens, were inoculated into Vero (African green monkey) cells
  • Three days later a distinct cytopathic change (focal rounding and refractility) was evident, and an aliquot of supernatant fluid was removed for negative contrast electron microscopy
  • In EM, large numbers of filamentous "virus" particles were seen which were approximately 100 nm in diameter and varied in length from 300 nm to more than 1500 nm
  • In all details, these particles were indistinguishable from Marburg "virus" particles studied in 1967 (isolates from Germany) and 1975 (isolate from South Africa)
  • Vero cells infected with the same "isolate" from Zaire were examined also by thin-section electron microscopy and the "virus" particles in these sections were identical to those observed in the 1967 and 1975 "isolates"
  • Although preservation of liver tissue was poor upon examination, large numbers of filamentous "virus" particles and inclusion bodies (masses of tubules) were found which were indistinguishable from those in Marburg "virus-infected" human and guineapig livers studied in 1967 and 1975
  • An antigenic difference between this isolate and Marburg '67 was demonstrated by indirect immunofluorescence (I.F.A.)
  • With the exception of a weak reaction to Marburg antigen at a 1/4 dilution of the Zaire convalescent serum, the
    new isolate was distinct from Marburg "virus"

When looking to either prove or disprove a positive claim, such as the existence of an Ebola "virus" as was the case in this particular instance, one must always look to the original foundational papers and see if the scientific evidence supporting the claim actually exists. Tracing the origin of the Ebola "virus" to its roots led me to three different papers by three different teams of researchers in three different parts of the world. It should come as no surprise to anyone who understands the pseudoscientific methods virology employs that, at no point in time, do any of the papers submitted adhere to the scientific method. This is absolutely essential in order for a study to be considered scientific. Nowhere in any of the papers is an Ebola "virus" ever properly purified and isolated directly from the fluids of a sick host, thus there is no independent variable for the researchers to vary and manipulate in order to determine cause and effect. Without a valid independent variable of purified/isolated particles, there can be no true pathogenicity studies utilizing a natural route of exposure, thus there can be no pathogenic claim. Without proper controls, there is no way to determine what other confounding factors could also potentially cause the effect one is searching for through experimentation, thus making the results obtained invalid and meaningless.

What these pseudoscientific researchers do instead is attempt to skirt around the scientific method by presenting manufactured indirect evidence as a stand-in for the real deal. They are con men selling counterfeit results. Instead of properly purified and isolated "virus," we get unpurified cell cultured soup mixed with many toxic ingredients such as Vero cells, medium 199, and 7.5% calf serum. Instead of observing the "virus," we get the non-specific cell death known as the cytopathogenic effect blamed on an invisible pathogen which can be a result of many things other than a "virus" such as changing the medium halfway through to one more suitable to producing the desired cytopathic effect. Instead of visualizing nothing but the particles claimed to be the new "virus," we get EM images of unpurified and non-isolated filamentous particles ranging wildly in shape and size which were previously associated with the Marburg "virus." We get histopathological lab results showing the same findings obtained through investigation with the Marburg "virus" a decade before. We get non-specific indirect antibody results used to claim that the "virus" is a new "virus" within the same family as the Marburg "virus" even though the other indirect findings should have led to the conclusion that they had either uncovered the same "virus" or that the results in both cases were fraudulent. In other words, the researchers found the exact same particles in EM images associated with cases of the exact same symptoms of disease attributed to Marburg (and many other diseases) yet as the antibody results did not align, rather than question the credibility of the previous Marburg findings, the researchers decided that what they had was a new "virus" instead. Anything to keep the story alive.

However, if one goes back to investigate the Marburg "virus," one would see the exact same pseudoscientific practices were employed where no "virus" was ever purified and isolated and the same particles belonging to rabies were identified instead as Marburg. If one looks into the rabies "virus," one will see this same pattern play out, and so on and so forth as this trail is traced back as far as it can go. The same cycle of deception persists where the same symptoms of disease are given a new name associated with similar and/or identical particles based on indirect and contradictory antibody results. What one will never find is direct proof for the existence of any "virus" which adheres to the scientific method. All one will ever find is pseudoscientific fiction passed off as scientific fact.

With all of that being said, let this stand as my response to anyone claiming that we must intentionally infect ourselves first in order to say that there is no scientific evidence for the existence of any "virus." This is asinine and absolutely backwards. The burden of proof is on anyone making the positive claim that a "virus" exists and they must provide the evidence supporting their claim in order to justify it. This logically requires that the scientific evidence for the existence of the Ebola "virus" is contained within the original research papers. I've done the hard work for these people and tracked down the original studies used to make the case for an Ebola "virus." I've shown that, at no point in time, was the scientific method ever adhered to nor were any particles assumed to be Ebola ever properly purified and isolated nor proven pathogenic in a natural way. If anyone disagrees with this assessment, I have a proposal. Please show me in the three papers I shared above where the scientific method was applied and adhered to from the very beginning. Show me where the researchers purified and isolated the "virus" directly from the sick host. Show me that the particles in the EM images are of only the "virus" and nothing else. Show me that these purified and isolated particles can make a suitable host sick in a natural way and not through injections of unpurifued toxins directly into the brain. Show me where the results are reproduced and replicated on a large scale utilizing the proper controls as should be expected of any scientific endeavor. If any person claiming the existence of an Ebola "virus" can show me where in these papers it was scientifically proven that the Ebola "virus" exists by adherence to the scientific method, then I will go to Africa to intentionally infect myself on my own dime. Granted, at that point they will have proven their case thus making my trip to Africa an expensive yet pointless and potentially dangerous endeavor for me. However, if they can not show that this evidence is contained within these three papers, they will concede that the scientific evidence proving the existence of an Ebola "virus" is nowhere to be found and I will look forward to a free first class trip to a safari in Africa.

Any takers?

ViroLIEgy
19 Sep 2022 | 3:47 pm

Antiviral


I am excited to announce the arrival of a weekly newsletter on Substack that I have titled "Antiviral." As I often write short pieces breaking down news articles and studies that I come across throughout the week, this newsletter will be a collection of these writings together in one place in a weekly format. The newsletters will contain information that I feel is important but unnecessary to write up as an in-depth article on viroLIEgy.com. Here is the type of content that you can expect:

  • Highlights and commentary on mainstream articles
  • Quick breakdown of relevant studies
  • Spotlights on different voices within the movement
  • New articles, podcasts, and interviews from the community
  • Any necessary responses to articles critical of the "No Virus" narrative
  • Sharable memes and quotes
  • Inside information on current projects
  • And even more in the pipeline

This newsletter will serve as an important compliment to the viroLIEgy.com site. Please support this endeavor by signing up for a monthly donation – that way you will be the first to know about all the latest developments. Not only that but it will help with some very exciting projects in development.  

https://mikestone.substack.com/

Thank you all for your continued support and for sharing this information far and wide. I wholeheartedly believe that by spreading our message through as many avenues as possible, we can reach those who are in need of hearing it. In turn, they can pay it forward and share what they learn in order to reach someone else. Together, we can and we will end this cycle of fear and instill hope for a better tomorrow for ourselves, our children, and for future generations. Together, we will bring about lasting change. ❤

ViroLIEgy
16 Sep 2022 | 3:14 pm

Dr. Mark Bailey Bids Farewell to Virology


I'm extremely excited to share Dr. Mark Bailey's latest essay on the fraud of virology. I know this one has been a long time in the making and has even expanded beyond its original scope. Mark is a brilliant researcher and has definitely outdone himself with his latest masterpiece. It clocks in at a full 67 pages of meticulously detailed analysis and investigation.

For those who may be unfamiliar with Mark (I imagine not too many are at this point), he is the other half of the virus-busting dynamic duo alongside his talented wife Dr. Sam Bailey. Together, they have produced many amazing and entertaining videos breaking down the absurdity of the "viral" pseudoscience. While Sam focuses on the video aspect of the equation and amusingly points out the ridiculous and illogical claims of virology, Mark has lasered in on writing equally important articles and essays detailing the extent of the fraudulent practices that are employed. However, he has done some excellent interviews and presentations himself as well as a very memorable debate with Kevin McCairn. He is also co-author of the "Settling the Virus Debate" statement with Dr. Kevin Corbett.

For an even greater insight into the man behind this brilliant essay, we can turn to the words of his wife Sam. From the biography section on their site:

Mark is the husband of Dr Sam Bailey and when you see one of them, you are really seeing both of them. They started working together when they first met in 2007 and have been a close team ever since. Mark and Sam are based in New Zealand and have three children together.

Since early 2020 he has been the duo's chief researcher with a focus on microbiology, the existence of viruses, as well as historical and epistemological issues within medical science.

Mark won an undergraduate scholarship to the University of Canterbury in 1994 and then completed his medical training at the University of Otago in 1999.

He worked in many specialties as a resident doctor and was also a clinical trials research physician for several years. In 2016 he left clinical practice due to dissatisfaction with the allopathic medical system. 

Mark is the author of "A Farewell To Virology (Expert Edition)" and co-author of "The COVID-19 Fraud & War on Humanity".

In his younger days Mark was seven-time New Zealand duathlon champion, three-time Le Race 100K cycling champion, and was one of the world's top 10 duathletes in his 20s. He still keeps in peak condition and even picked up a New Zealand cross-country running title as a veteran.

About Dr. Mark Bailey
A brilliant investigator and a top 10 worldwide duathlete as well?!?! I'm starting to think Mark may be Batman… 🤔

Presented below is the abstract from Mark's essay which offers an incredible summation of the problems inherent in virology. After reading this preview, please download and read the rest of Mark's essay as it is a truly engaging and eye-opening experience:

A Farewell To Virology (Expert Edition)

Virology invented the virus model but has consistently failed to fulfil its own requirements. It is claimed that viruses cause disease after transmitting between hosts such as humans and yet the scientific evidence for these claims is missing. One of virology's greatest failures has been the inability to obtain any viral particles directly from the tissues of organisms said to have "viral" diseases. In order to obfuscate this state of affairs, virologists have resorted to creating their own pseudoscientific methods to
replace the longstanding scientific method, as well as changing the dictionary meaning of words in order to support their anti-scientific practices. For instance, an "isolated" isolate does not require the physical existence of the particles in order to be afforded "isolation" status.

A viral particle must fulfil defined physical and biological properties including being a replication-competent intracellular parasite capable of causing disease in a host such as a human. However, "viruses" such as SARS-CoV-2 are nothing more than phantom constructs, existing only in imaginations and computer simulations. In this paradigm, cases of invented diseases like COVID-19 are nothing more than the detection of selected genetic sequences and proteins purported to be "viral." The existence of a virus is not required in this loop of circular reasoning and thus entire "pandemics" can be built upon digital creations and falsely sustained through in vitro ("test tube") molecular reactions.

This essay contains three parts. Part One outlines some of the history of virology and the failures of the virologists to follow the scientific method. The many and far-reaching claims of the virologists can all be shown to be flawed due to: (a) the lack of direct evidence, and (b) the invalidation of indirect "evidence" due to the uncontrolled nature of the experiments. The examples provided cover all major aspects of the virological fraud including alleged isolation, cytopathic effects, genomics, antibodies, and animal
pathogenicity studies.

Part Two examines the fraud used to propagate the COVID-19 "pandemic." A breakdown of the methodology relied upon by the original inventors Fan Wu et al., shows how the fictional SARS-CoV-2 was "created" through anti-scientific methods and linguistic sleights of hands. It is part of an ongoing deception where viruses are claimed to exist by templating them against previous "virus" templates. Using SARS-CoV-2 as an example, the trail of "coronavirus" genomic templates going back to the 1980s reveals that none of these genetic sequences have ever been shown to come from inside any viral particle — the phylogenetic trees are fantasies. The misapplication of the polymerase chain reaction has propagated this aspect of virology's fraud and created the 'cases' to maintain the illusion of a pandemic.

Part Three provides an analysis of how some key participants, "health" institutions, and the mainstream media maintain the virus illusion through information control and narratives that parrot virology's claims. By way of happenstance, the virological fraud now finds itself front and centre of the COVID-19 fraud. From here, however, it can be critically appraised by those outside virology and the pseudo-scientific paradigm virology has built around itself can finally be dismantled and laid to rest.

The aim of this essay is to provide refutations to various claims that pathogenic viruses exist and cause
disease. SARS-CoV-2 has been used as the main example but the principles apply to all alleged viruses. What follows addresses virology's often arcane literature on its own terms, which, it should be said, may make parts of this essay somewhat heavy reading. However, it is hoped that this contribution will fill a niche for the reader seeking a more technical understanding of the virus hypothesis as it seeks to expose the very foundation of purported pandemics and fraudulent medical practices. The threat of virology to humanity is increasing so it is time we bid farewell to these destructive pseudoscientific practices and free ourselves from unnecessary fears.

A Farewell To Virology (Expert Edition)

Update: For anyone looking for the abridged version of Dr. Mark Bailey's fantastic "A Farewell to Virology," Eric Coppolino and I compiled some of the best quotes from the 67-page essay. While it was difficult to wittle down and I highly recommend reading the whole masterpiece, we got it to a 19-page Word document that can act as a highlight reel of goodies!

Click to access farewell-to-virology-excerpts.pdf

Credit for the amazing photo of Mark crushing it goes to William Huston

I also want to highlight Mark's earlier takedown of the "Covid" hoax where he and co-author Dr. John Bevan-Smith broke down the global deception by highlighting the four fraudulent pillars of virology. Please download and enjoy this earlier fantastic 46-page essay:

The COVID-19 Fraud & War On Humanity

COVID-19 is a fraud because its alleged causal agent, a purported novel coronavirus called SARS-CoV-2, has not been proven to exist in nature and therefore has not been established as the cause of COVID-19, the disease and pandemic invented by the World Health Organisation (WHO). For the selfsame reason there are no variants of the "virus", which likewise exist only hypothetically in computers, cloud-based gene banks and in the minds of innocent people who have been comprehensively gulled by their governments.

The COVID-19 fraud, with its numerous preposterous claims, constitutes nothing less than a war on humanity by organisations such as Anser, Fors Marsh, and Palantir that conduct the scam through Big Pharma, with its backers and enablers, including the World Economic Forum, the Bill and Melinda Gates Foundation, the WHO, technology conglomerates, the mainstream media, complicit governments, and COVID "pirates" such as UNC Chapel Hill and Imperial College London, to a one beneficiaries of the fraud.

COVID-19 is a war on humanity because politicians and their governments continue to use this imaginary disease to terrorise and imprison their citizens, denying them guaranteed human rights and freedoms, and violating their once inviolable bodies with highly experimental and hazardous injections that contain a computer-generated spike protein mRNA sequence that instructs the body to poison itself. These nefarious injections, which also contain undeclared non-biological objects for undeclared purposes, are injuring millions and killing many thousands of people around the world, including up to 245 New Zealanders as at 5 November 2021.

A virological fraud lies at the heart of these crimes against humanity – that SARS-CoV-2 has never been physically isolated or shown to be the aetiological (causal) agent of COVID-19. In this article, the authors examine the illusory world of virology to explain how a virus that no one has seen or knows where it has come from, that no one knows what it does or where it is going, is, according to the fraudsters, stealing across borders and boundaries and coming to get you no matter where you are. How can it be, the authors ask, that this phantasmagorical madness has morphed into a world redolent with fear in which democratic governments have abandoned democratic principles to engage in the control and "deletion of human beings" that may be just a "variant" away from turning into World War III?

THE COVID-19 FRAUD & WAR ON HUMANITY

Dr. Sam Bailey also provided three really great companion videos where she read Mark's first essay with some added visual flair. For those who may not want to stare at the tiny print on the computer screen, watching Sam and listening to her lovely voice may be the preferred way to experience this one. Maybe she will do a reading for the new essay with enough demand (hint hint). 😉

ViroLIEgy
14 Sep 2022 | 4:09 pm

Keeping the Truth Movement True with Patrick Gunnels and Eric Coppolino


Yesterday, Eric Coppolino and I were invited to the "Reading Epic Threads" show with Patrick Gunnels to discuss unity and disunity in the truth movement and where to draw the line. We also focused on whom to trust in the medical freedom movement as well as how to decide how far to go when trying to awaken people. It was definitely a fun conversation to take part in. Hopefully this can help in the understanding of why we need to always verify where and from whom we are getting our information from.

https://rumble.com/v1jy3p5-keeping-the-truth-movement-true-coppolino-and-stone-join.html

You may also remember Patrick from his recent debate with Steve Kirsch, which definitely did not go too well for Steve. I highly recommend watching as I feel Patrick did a masterful job keeping Steve on topic and exposing the flaws in his "logic:"

ViroLIEgy
9 Sep 2022 | 3:41 pm

Setting the Record Straight With Regis Tremblay


After everything that happened with the Poornima Wagh situation, there seemed to be a lot of confusion and anger over how the events transpired. Fortunately Regis Tremblay, the man who introduced Poornima to audiences, was more than happy to let this be a two-sided conversation in order so that both parties involved could share information with those who still had unanswered questions. This way, people could weigh the evidence and decide for themselves, which is a fair and balanced approach. Regis was also kind enough to have us on to talk about our own efforts to get the message out on the fraud of virology. I wanted to provide these interviews in one easy to find place. I also want to thank Regis for allowing us a voice on his platform. I feel that he handled this situation in a very honorable fashion and I appreciate his willingness to share our stories with the world at large.

Poornima Wagh Takes the Stand to Defend Herself

Accused of being a fraud, charlatan and pathological liar, Poornima asked to defend her self. I am not going to judge because I do not have the wisdom of Solomon, nor a crystal ball. I have invited her accusers to come on the show Sunday or Monday to present their position.

Eric Coppolino's and Bill Huston's articles are here:


https://planetwavesfm.substack.com/p/charlatans-web

https://apocalypticyoga.substack.com/p/poornima-wagh-is-a-fraud

Investigating Poornima Wagh

Eric Coppolino, 39 year investigative reporter discusses his background and research in "vetting" Poornima Wagh. He is a specialist in mass poisoning incidents and associated lawsuits.

He is the founder and editor of Covid19 News, and the author of the Covid Chronology, a day-by-day account of lockdowns and claimed pandemic back to 2006. He hosts Planet Waves FM on the Pacifica Network and has covered covid every day for the past 916 days.

Three Team Members Who Vetted Poornima Wagh

William Huston, Christine Massey, and Mike Stone share their participation in the vetting of Poornima Wagh, their thoughts, reasons, and feelings about this unfortunate situation.

The Pseudoscience of Virology

Mike Stone talks about "Virology" as a Pseudoscience. His website, www.viroliegy.com is an important resource of EVERYTHING related to Covid-19 SARS-2″ viruses, masks, PCR tests, the transmission myth, and much more.

200 FOI Requests – 40 Countries: No Evidence SARS-CoV-2 Exists

Canadian biostatistician, Christine Massey, has accumulated FOI requests from over 200 institutions in 40 countries: not one has proof of any scientific papers, using legitimate methods, that SARS-CoV-2 exists.

Also the No Virus Challenge, an organic group of doctors, scientists, and lay people showing that there is no proof viruses exist. Her website: www.TinyURL.com/NoRecordFound

ViroLIEgy
6 Sep 2022 | 3:23 pm

Under the Microscope With the Fakeologist


It is not my intention to draw out this situation with Poornima Wagh. However, many have had questions about how certain events transpired and why we felt we needed to verify her credentials as well as the claims she had made regarding the groundbreaking research into 1,500 "SARS-COV-2" samples and the work with 18 scientists around the world investigating the contents of vaccines. I already explained the importance a few days ago in the article A Matter of Trust but it is apparent that many still have questions. Sadly, we all do at this stage. I will be posting a collection of interviews later in the week that myself and others tied to this situation have done with Regis Tremblay. The Fakeologist also reached out to me yesterday to see if I could clear up some of this confusion. It was a good conversation that hopefully can help shed some light for anyone who may still be confused. My hope is that we can all come together and move beyond this unfortunate chain of events and get back to focusing on exposing the pseudoscience known as virology.

FAK606-Mike Stone on Poornima Wagh
ViroLIEgy
4 Sep 2022 | 4:27 pm

A Matter of Trust


"Tell a lie once and all of your truths become questionable."

-Unknown

Dr. Stefan Lanka. Dr. Tom Cowan. Dr. Andrew Kaufman. Dr. Sam Bailey. What do these four people, at the forefront of the "No Virus" movement (if we can call it that), have in common besides a tireless quest to present the truth about the fraud of virology? They do not claim to be something or someone that they are not. Each of these doctors have credentials and work experience that can be easily verified. They have all worked hard to gain our trust by being open and honest regarding their professional backgrounds. In spite of this, each of them have had their names run through the mud by mainstream media outlets and alternative news sites in attempts to discredit and debunk their work. Fortunately, these professionals have each been able to stand tall in the face of inaccurate, misleading, and erroneous allegations made against them due to the fact that they all have nothing to hide. While they have each faced the adversity and proven their detractors wrong while coming out stronger for having done so, that does not appear to be the case for relative newcomer Poornima Wagh.

I did not want to write this as I really do believe Poornima Wagh has been through a smoldering ring of fire as of late. Sadly, it is an inferno that she seemingly created for herself through her own actions. In any case, it is not my intent to pour on the metaphorical lighter fluid and fan the flames. However, due to the response that I have seen to the vetting of Poornima, I felt that it was necessary to present the case for why it was imperative that Poornima's claims and credentials were ultimately verified. I want to also ask those who found themselves under the spell over the last few months to use this unfortunate situation as a much-needed wake-up call in order to re-evaluate those that they view as trustworthy. It is easy, especially during these challenging times, to look for and cling to a savior, the expert in shining armor ready to slay the legendary "viral" beast. When one seemingly steps out from behind the shadows, it is easy to push aside and abandon all critical thought and healthy skepticism in order to latch onto the savior with welcoming and open arms. However, if one takes a moment to step back and view the savior with the same discernment and logic that led them to see through the "viral" delusion in the first place, they will many times see that these saviors are sadly not who they claim to be. Unfortunately, it appears as though this trust that was easily given by many may have been entirely misplaced in Poornima Wagh.

As with Brian Ardis and his snake venom presentation a few months ago, Poornima Wagh burst onto the scene and took the "truther" community by storm in early July with an engaging presentation debunking virology on the Regis Tremblay podcast. Proclaiming herself as a virologist with 2 simultaneous PhD's (one in virology and the other in immunology) from the prestigious London School of Hygiene and Tropical Medicine, Poornima had the impressive credentials which immediately made people take notice and listen. It didn't hurt that Poornima also announced that she led a monumental study that contained the very evidence needed to not only prove "SARS-COV-2" did not exist but also that virology and germ theory were a complete fraud. She also promised future presentations debunking PCR, masks, and the vaccines as well. A dual PhD virologist seemingly coming out from nowhere with the very evidence needed to shut down this lie once and for all almost seemed to be too good to be true.

Poornima did deliver on the promise of the follow-up slide-show presentations. In fact, a lot of the information that Poornima presented during her three appearances on the Regis Tremblay show was factual and did a great job illustrating the faults in germ theory, virology, and the health response to this "pandemic." She shared information from many sources, including some of my own, which makes this a very difficult article for me to write. While there were many truths in the information Poornima shared, there were certain elements that stood out from a factual and scientific standpoint that undermined her credibility as someone with dual PhD's in virology/immunology and 20 years of lab experience. While I do not want to belabor technical errors as I am sure I make them myself (granted, I do not claim to be a virologist), there were erroneous statements made by Poornima about methods used by virologists which she should have known better than to make.

As a quick example, during her most recent presentation with Dr Wai-Ching Lee, Poornima made two alarming statements related to the cell culture process that a person with her position and experience should not make. She claimed in this slide under # 2 that both Vero cells and HeLa cells are cultured together with the lung fluid taken from a sick patient:

This is false as different cell lines (such as monkey kidney cells and human cervical cancer cells) are never mixed together with the lung fluid and then cultured.

In the following slide with # 4, she stated that trypsin is added during the culturing process:

This is another erroneous claim as trypsin is used after the cell culturing process takes place in order to detach the cells from the cell culture flask, often in the case of passaging the cells to a fresh vessel. Trypsin is not added in during the actual culturing of the "virus."

There were other errors and questionable statements that Poornima made throughout her interviews and presentations that raised red flags for many of us watching on the sidelines. As I said, it is not my intent to pile on Poornima regarding these points. However, they were ultimately crucial as they served as evidence to us that Poornima may not hold the required credentials and experience that she claimed to possess. Due to these growing questions and concerns, it was felt that it was time to address these issues with Poornima in order to properly vet her.

Missing PhD's and Thesis
https://www.bitchute.com/video/6uY601hwZIId/

"Anybody asking about my credentials, here are my credentials, you can check them out…and…you can give these colleges a call and I'm sure they can help you out with this."

-Poornima Wagh

As can be seen by Wagh's statement, she openly invited anyone doubting her credentials to verify her claims by calling the colleges she said she had attended for themselves. That is exactly what investigative journalist Eric Coppolino did after a 45 minute pre-interview with Poornima raised even more questions than answers. While I will not rehash his story, (you can read it here), I want to provide the responses he received regarding Poornima's claim of aquiring two PhD's in virology and immunology in just 3 years using one thesis (a phenomenal and unrealistic feat) from the London School of Hygiene and Tropical Medicine:

"The London School of Hygiene and Tropical Medicine has checked in with the following statement this morning from their press office: "Nobody by the name of Poornima Wagh has obtained a degree from our institution." We have also received a second confirmation from Roger Watson"I have it from the dean of Faculty of Infectious and Tropical Diseases at LSHTM, Alison Grant, that nobody of her name has obtained any degree from their institution." Update Thursday, September 1: The London School of Hygiene and Tropical Medicine has confirmed: "Nobody with the last name Wagh, including as part of a hyphenated surname or as part of a surname containing the letters in that order, has obtained a degree from this institution."

The very school that Poornima claimed to receive her dual virology/immunology PhD's from stated that they have no record of anyone by that name or any variations thereof having ever attended nor receiving PhD's from their institution. Searches for Poornima's thesis paper, which would have been a requirement in order to attain the PhD's and would be public record, came up fruitless. In other words, Eric (along with the help of Dr. Kevin Corbett and Roger Watson) did exactly what Poornima asked any of her doubters to do. He checked with the institutions and found no record of her attendence, PhD's, nor her thesis. Needless to say, this is a major red flag that was in dire need of resolving in order to establish some semblance of trust in the professional background Poornima presented.

Update: I have had a few people question why Eric Coppolino was able to receive information about Poornima Wagh not attending LSHTM without her permission. I decided to follow-up with LSHTM to find out. It seems that due to Poornima claiming affiliation with the institution, they were able to release this info about her non-attendence under special circumstances.

The 1,500 "SARS-COV-2" Samples Study
The above three slides are all from Poornima's first presentation on Regis Tremblay's show.

Another aspect of Poornima's story that caused alarm for many of us was her extraordinary claim of having led the testing of 1,500 "SARS-COV-2" samples from southern California and finding nothing in them at all, just cellular debris. According to Poornima's recounting of events, she was contacted by her P.I. in April 2020 to do the testing of 1,500 "SARS-COV-2" positive samples as her university had received a $1.5 million grant from the NIH to find and isolate "SARS-COV-2" from these samples. Poornima insisted that she was reluctant to take on the project as she knew that she would find no "virus." However, after continued prodding by her P.I., Poornima agreed to perform the procedures but only upon the condition that she were allowed to do the process her way "as a pathologist" adhering to Koch's Postulates. Upon finding no "SARS-COV-2" in any of the 1,500 samples as well as being unable to make any ferrets sick with the materials, her P.I. requested that Poornima and her team of 20 lab members repeat the entire process all over again, for a grand total of a three times. The results remained the same that no "SARS-COV-2" existed in any of the samples and no animals became sick. Alarmed by these results, the P.I. reached out to 100 differemt labs around the country to see if they could recreate the findings as well. Only 6 labs responded, 5 in California and one on the East coast. All labs followed the exact same protocols as laid out by Poornima and found the exact same results as well.

This led to a contentious meeting with the CDC's Robert Redfield who demanded that, regardless of the findings, they all needed to state that "SARS-COV-2" was found within the samples. According to Poornima, her lab refused to follow along and attempted to publish the results as they were. There were numerous unsuccessful attempts with over 21 different journals, the last occuring in Oct. 2021. During this process of attempting to get the study published, the FBI raided her lab in April 2021 and confiscated everything. Poornima claimed that 5 members, including herself, kept digital and paper copies of the study and have continued the search for a publisher ever since, currently seeking publication in India. Apparently, two members of her team committed suicide under suspicious circumstances and according to Poornima's interview with Eric Coppolino, her P.I. mysteriously died a few days before they spoke.

Needless to say, this story is incredible, and if true, it would be the death knell not only for "SARS-COV-2" but also for the pseudoscience known as virology. In fact, when many of us heard these claims, we were excited by the possibility that the No "Virus" Challenge was unnecessary as the proper controls and procedures that we wanted to see were already carried out by various labs and completed. However, upon closer examination of Poornima's story, there are serious red flags which cast even more doubt about her credibility.

Over the course of this pandemic, a nearly identical version of Poornima's story has made the rounds over social media, even being "fact-checked" numerous times. This version of events tested 1,500 "SARS-COV-2" positive samples and found mainly Influenza A along with a smaller number of Influenza B within the samples rather than "SARS-COV-2." This particular narrative was credited to various people, including a seemingly fictional Dr. Derek Knauss as well as a very real Dr. Robert Oswald who denied any involvement. Even Partick Gunnels, who recently debated Steve Kirsch over the non-existence of "viruses," was credited as the virologist after he read the story on YouTube. In order to show the striking similarities between Poornima's story (right down to the dual virology-immunology degrees) and the previous version which has circulated at various times, I am providing the words attributed to Dr. Derek Knauss from April 19, 2021:

"A clinical scientist and immunologist-virologist at a southern California laboratory says he and colleagues from 7 universities are suing the CDC for massive fraud. The reason: not one of 1500 samples of people tested "positive" could find Covid-19. ALL people were simply found to have Influenza A, and to a lesser extent Influenza B. This is consistent with the previous findings of other scientists, which we have reported on several times.

Dr. Derek Knauss: "When my lab team and I subjected the 1500 supposedly positive Covid-19 samples to Koch's postulates and put them under an SEM (electron microscope), we found NO Covid in all 1500 samples. We found that all 1500 samples were primarily Influenza A, and some Influenza B, but no cases of Covid. We did not use the bulls*** PCR test.'

At 7 universities not once is COVID detected

'When we sent the rest of the samples to Stanford, Cornell, and a couple of the labs at the University of California, they came up with the same result: NO COVID. They found Influenza A and B. Then we all asked the CDC for viable samples of Covid. The CDC said they can't give them, because they don't have those samples.'

'So we came to the hard conclusion through all our research and lab work that Covid-19 was imaginary and fictitious. The flu was only called 'Covid,' and most of the 225,000 deaths were from co-morbidities such as heart disease, cancer, diabetes, pulmonary emphysema, etc.. They got the flu which further weakened their immune systems, and they died.'

'This virus is fictitious'

'I still need to find one viable sample with Covid-19 to work with. We who conducted the lab test with these 1500 samples at the 7 universities are now suing the CDC for Covid-19 fraud. The CDC still has not sent us a viable, isolated and purified sample of Covid-19. If they can't or won't, then I say there is no Covid-19. It's fictional.'

'The four research papers describing the genome extracts of the Covid-19 virus never managed to isolate and purify the samples. All four papers describe only small pieces of RNA that are only 37 to 40 base pairs long. That is NOT a VIRUS. A viral genome normally has 30,000 to 40,000 base pairs.'

https://shiftfrequency.com/at-7-universities-not-once-is-covid-detected/

Update: Bill Houston, who wrote a very good article breaking this Poornima situation down, had previously uncovered this reply on a forum apparently from Poornima 2 years ago:

https://creation.social/u/lisawarren?offset=9

As can be seen, Poornima claims that she isolated Influenza A/B from the samples which aligns her story exactly with the Derek Knauss/Robert Oswald story that had stated the very same thing. That is, until Poornima changed it to no "virus" having been found within the samples whatsoever.

The striking similarities between the stories of Poornima and Derek Knauss and Co. were a huge red flag. This nearly identical tale attributed to various people over the last year-and-a-half has popped up numerous times yet there is no verifiable information that these studies and events ever took place. This leads to one of two possible scenarios:

  • Poornima is finally giving us the real version of these events.
  • Poornima copied this story and incorporated it into her own after having read it.

Taking into consideration that Poornima has seemingly not been honest about her PhD's, it leads one to conclude that the most likely scenario is the latter.

Worldwide Vaccine Investigation
The above 5 slides relate to Poornima's current worldwide vaccine investigation. https://www.bitchute.com/video/6uY601hwZIId/

One of Poornima's most recent unverified claims is that she is currently engaged in a worldwide investigation into what is really contained within multiple "Covid" vaccines. She stated that the investigations have so far uncovered that all of the vaccines contain essentially the same ingredients (just in varying quantities) which includes lipids nanoparticles, trillions of reduced graphene oxide particles, and an assortment of heavy metals. Not a single vaccine contains mRNA, even the Pfizer and Moderna injections. Poornima listed 18 scientists stationed in various parts of the world collaborating with her in this endeavor yet she has not provided any verification beyond that. I have it on good authority that, while Poornima claimed to have 2 scientists in New Zealand, no one in NZ is working with her which casts a shadow of doubt upon the whole operation. When we include the unverified claims regarding the questionable vaccine investigation with both the missing PhD's and the apparent plagarism of the lab story, this confluence of highly suspicious information needed immediate clarification from Poornima. However, this sadly was not meant to be.

If I'm a fraud, then I'm a fraud. I'm gonna go down with that. That's fine. That's fine. I'm sorry Regis, maybe you are disappointed in me.

-Poornima Wagh

Regis did invite Poornima back on after Eric's article so that she could defend herself from the evidence presented against her. While I was not expecting anything different than what ultimately transpired, there was a part of me that had hoped that maybe this was just one big misunderstanding and that Poornima would somehow come through with documentation proving that she did in fact attain 2 PhD's from LSHTM. Maybe she would present her thesis paper and provide availability to anyone anxious to read it. Perhaps she would give a small taste of the methods section from the monumental study debunking "SARS-COV-2" and virology that she was looking to publish independently in India. A part of me was pulling for her to give us something. Anything, really.

Unfortunately, all that was given was an inaccurate portrayal of the events that transpired. Poornima stated that this was an attack against her based on our collective ego. She continued to falsely claim that Eric grilled and interrogated her. Poornima stated that she was harassed (which is untrue as can be seen by Christine Massey's release of our e-mails with her here) and she even threatened legal action. When pressed by Regis if she would allow him, someone whom she considered a friend, access to her school records in order to clear this situation up once and for all, Poornima said that she would not let Regis nor anyone else see this evidence. Throughout the 42 minute interview, Poornima oddly and repeatedly referred to herself as a fraud while trying to defend herself against this perception and even apologized to Regis for disappointing him. It is hard to make the case that these were not the words of someone with everything to lose and nothing to gain by verifying the accuracy of her professional background and education. For someone who originally seemed open to being vetted, Poornima ended up not being agreeable to it at all.

This unwillingness to be vetted is a major concern when a person has made some extraordinary claims that are in need of being verified. Please note that had Poornima never claimed to be a dual PhD in virology and immunology, had never claimed to have led a ground-breaking study disproving all of virology, and had never claimed to be working with 18 labs across the world dissecting the vaccines, the need to verify her background would have been unnecessary and the focus would have been solely on the information she presented. However, Poornima made her credentials and her expertise central to her own credibility by making such bold statements and tying it into her own personal story and presentations. Extraordinary claims demand extraordinary evidence to back them up and so far, Poornima has delivered nothing to verify that these claims are in fact true. If we accept these claims as true without investigating them, then we are doing a disservice to ourselves and everyone else. I had reached out to Poornima after Eric's article but before her last interview with Regis to explain this to her and to see if she would accept another chance to get together to talk and clear the air:

Hi Poornima

This is Mike from ViroLIEgy.com. I wanted to reach out as it seems things have become a little contentious between you and others within an email group I participate in. I understand from some communications that you felt grilled by Eric in his pre-interview and also threatened by inquiries into your past education, work experience, and credentials. It is unfortunate if our communications with you have come across in such a manner. No one wants to claim you as a fraud and we are in fact holding out hope that the work you have done is legitimate as it would be a great boost to our collective cause.

Please understand that our attempts to vet you are based upon obtaining verification before promoting your work. As you have set your credentials and experience as a central component to the credibility of much of what you present, we need to verify this before we would be able to jump on board. We want nothing more than to come together as a unified front. However, there are some definite questions and concerns we would love to address with you and resolve in order to move the conversation forward. Please do not see this as a threat or attempt to discredit/defame you as that is definitely not the intention. We really need to be able to verify as much as we can as we would be doing a disservice to ourselves and everyone else without doing our due diligence. I hope that we can all get together and discuss this in the interest of becoming a united front. Thanks for understanding and also for promoting my blog in your presentations. It is greatly appreciated. 🙂

-Mike

Sadly, I never heard back from Poornima. However, as she stated in her latest interview with Regis, Poornima is right in that she owes us nothing. Even though she agreed to it, Poornima does not need to meet with us. She does not need to verify herself for us. She does not need to explain her motivations to us nor to anyone else. This was entirely voluntary and was never a requirement. However, doing so would have been a great way to foster a relationship of trust between us as well as with anyone else who listens to her. It would have laid a strong foundation that could have been built upon going forward.

Speaking for myself, I wanted to believe in Poornima. I wanted to promote her presentations. I wanted another ally in this fight. I wanted very much to proclaim that the necessary control experiments that could serve as the final nail in the coffin of virology were already completed and ready to be shared. I understand the strong desire to believe in someone. I understand the promise of what Poornima represented and the hope that she inspired. I understand also, that as one of the messengers who is shining a light on the cracks in the foundation of her personal story, I will be blamed by those supporters who are angry for dashing the promise she embodied. However, as I stated in my email to Poornima, I would be doing a disservice to myself and to everyone else if I did not do the due diligence of helping to vet her information properly. We owe it to ourselves to always ensure that the information we receive and share is accurate, and with Poornima, determining this accuracy was heavily tied to having her verify her credentials. Without the PhD's, her whole story falls apart.

In the end, it all comes down to a matter of trust, which is something that is earned and not given. It is built by the integrity and the honesty of the other person. It is based on the consistency of telling the truth. If trust is earned and that relationship is ultimately broken, it is a difficult thing to repair and rebuild. Thus, it is of the utmost importance that those who are presenting valuable information to the public regarding the fraud of virology are shown to be trustworthy by demonstrating themselves to be consistently honest and of the utmost integrity.

In my own personal example, I try to be as open and honest about myself as possible. I am not claiming to be any more than I am. I have no problem if someone decided to call my college and ask if I actually obtained a degree in Exercise Science. I have absolutely nothing to hide and I feel better being upfront about who I am. While I have spoken about my educational background, it does not enhance nor detract from the information I share. It is not essential to my writing about the foundational flaws of virology as this information stands on its own and is in no way tied to my background. Anyone looking into my background will never be able to gather evidence that I lied about who I am as I value honesty above all else. If, for some reason, I did lie and it was uncovered, this information would rightfully be used against me, showing a dishonest person who has stained everything he wrote. Sadly, it would also be used to paint anyone saying similar things as myself in a negative light as well. For example, this is how Steve Kirsch is using this situation with Poornima to attack us "virus deniers" in a recent blog post:

"Eric Coppolino found exactly the same thing Jessica did: she's a total fraud. This is why Poornima was so camera shy.

He wrote a brilliant Substack about it.

What we still don't know is why she is fabricating all this stuff.

I have the same problem with any of the leaders of the "virus denier" movement. Tom Cowan, Sam Bailey, Mark Bailey, Andrew Kaufman, Jon Rappoport, and others are all camera shy. There's a reason for that: they would be exposed as frauds in minutes."

Being exposed as dishonest would break a hard-earned chain of trust that has been established by myself, my colleagues, and those who have come before us. It is a chain that needs to remain unbreakable for those who will come after us. This is bigger than any one person as we are all links in this chain of transformational information.

In order to ensure that this chain remains unbreakable, we must establish that those who are attaching themselves to it are trustworthy as well. To do so, we must determine if that person is truthful. A great way of doing so beyond verifying records is to ask ourselves how we would respond if we were to find ourselves in a similar situation. If I was a dual PhD in virology and immunology, I'd be estatic to flaunt that information for anyone to see as, like it or not, it would make me more credible in the eyes of many. I would not shy away from providing this evidence if asked, especially if I was involved in a groundbreaking study and I needed to sell my own credibility in order to get more eyes on this research. If I was having trouble getting my study published and I knew this information was of vital importance as it could potentially end this fraudulent field once and for all,  I would create my own website and self-publish. I would also share the study with those who have a large audience in order to disseminate this information far and wide, especially if I felt that my life was potentially in danger due to a previous FBI raid and several mysterious deaths to my team members and P.I.

What I would not do if I was in this position is state that anyone can look into and verify my background and then get angry when someone finally does so. I would not back away from answering detailed questions about my groundbreaking study, my extraordinary story, nor my varied work history. I would not continue to look to publish my study in medical journals after numerous unsuccessful attempts to do so. I would not attack those who are my potential allies who were trying to vet my story by doing what anyone with common sense would do by asking for verifiable proof. If I was accused of lying about my credentials, I would not go on to do an interview defending myself where I do not provide the evidence in question. I also would not refuse to verify for the host that my credentials actually exist. Most importantly, I would not repeat that "I am a fraud" over and over again and apologize to the host who introduced me to the world at large for disappointing him. I would never accept the label of a fraud and I would fight to reclaim my credibility.

We must all ultimately determine for ourselves who we view as individuals that we can trust. We must always seek to verify the information that we receive by looking at the evidence for ourselves and judging it based upon its merits and our own personal standards. If we are to look at the facts relating to this unfortunate situation, what we find is:

  • The LSHTM stated that no records exist of anyone by the name of Poornima Wagh ever attending or receiving two PhD's from them.
  • Poornima's reluctance to verify and share any evidence of her PhD's, her thesis, or her studies.
  • The lack of any corroborating evidence for any study being performed looking at 1500 "SARS-COV-2" samples and finding no "virus."
  • No evidence of any raid by the FBI.
  • No evidence that Poornima is working with 18 other scientists around the world dissecting the vaccines.

These facts alone are enough, if my opinion, to break the chain of trust with Poornima. However, is it enough for anyone else? That is a personal question and one that we each need to evaluate for ourselves in order to answer. However, it is absolutely imperative to remember that for any individuals whom we hoist up into a position of influence, we must know for a fact that they are indeed who they say that they are and that they possess an honesty and integrity of character that will always shine through. We need to ensure that when someone comes along making amazing claims, before we put them into the spotlight, we slow down and verify that they are who they claim to be and that the information they claim to have actually exists.

At this fork in the road, there really are only two paths that can be taken, and the decision ultimately resides in Poornima. In light of the evidence supplied by the LSHTM, if the information was somehow inaccurate and Poornima does indeed have evidence of her two PhD's and her schooling there, she really should come forward with this evidence in order to put this issue to bed. It would also be wise to at least present some evidence relating to the monumental study involving the 1,500 "SARS-COV-2" samples as well as anyone who can corroborate that she is actually working with various labs around the world looking into the vaccines. At least some verification of her claims is required in order to reestablish the chain of trust.

The other option, if it ultimately does turn out that Poornima was dishonest about not only her credentials but also the research that she was supposedly involved in, is to simply come clean and apologize. While the trust would be broken and the damage to her credibility would be severe, it is a massively important first step towards repairing what was broken. If Poornima desires a voice in this movement, it is absolutely necessary to work towards rebuilding that trust.

What is sad about this situation is that Poornima has shown that she has a very good knowledge base and she is obviously gifted at doing power point presentations. She was able to capture the attention of many as she has a way of presenting information in an easily digestible manner. If she did lie about her credentials as well as her work, it was absolutely unnecessary as she did not need that false facade in order to be a voice in this movement. All she needed was to be herself, whoever that ultimately is, and present accurate information to the public. Would she have captured the attention of so many so quickly without the 2 PhD's and the groundbreaking studies? Probably not. However, while it may have taken a while longer to find an audience, her natural charm and style would have found a way to reach those seeking this knowledge. In the end, we would have witnessed the arrival of a powerful ally in this fight irregardless as to whether she was a virologist or not. Now, we may never know what could have been.

ViroLIEgy
29 Aug 2022 | 5:08 pm

The Marburg “Virus:” Precursor to Ebola


Most of the known viral diseases were excluded and the infectious agent was shown to be a hitherto unknown virus with many peculiar characteristics: it infects guinea pigs but not adult mice and is larger than known viruses and of different shape.

Preface to Marburg Virus Disease by G. A. MARTINI • R. SIEGERT

If you've been paying attention to the mainstream media for some reason, you're probably well aware of the re-emergence of many different "viruses" seemingly sprouting up around the world over the last few months. We've seen the oddly accurate prediction of the monkeypox in May 2022, the threats of oscure "viruses" such as nipah/langya, hantavirus, strawberry hepatitis A, the tomato flu, and the apparent reappearance of polio. One of the other lesser known "viruses" currently making the rounds in the media is known as the Marburg "virus." While it may not be as scary sounding to those who are unfamiliar with it, the "virus" has a close relative whose name may be enough to strike fear into the hearts of the ignorant. For those who do not know, the Marburg "virus" is the original incarnation of the Ebola "virus." My guess is you may be more familiar with the latter of the two.

In recent weeks, there have been reports of the Marburg "virus" making its presence felt in Ghana, a place which has never reported a case of the deadly "virus" before. Sadly, not only did Ghana report its first Marburg case early July 2022, they also reported their first deaths associated with the disease:

"An outbreak of Marburg fever has been detected in Ghana, whereas West Africa had been free of cases except for one case in Guinea in 2021. Currently, 98 people are considered contacts and are in isolation. No cases of Marburg fever have yet been detected among these contact cases.

So far two unrelated men have had Marburg fever. Presenting symptoms such as diarrhea, fever, nausea and vomiting, the two men, aged 26 and 51, have both died."

https://unric.org/en/marburg-virus-disease-origins-and-symptoms/

If you listen to the mainstream media, you may be convinced to believe that the Marburg "virus" is a "highly contagious, highly virulent" and deadly disease ready to burst forth and become the next epidemic in need of fearing:

The life-threatening virus is highly contagious, and has no known cure or approved vaccine.

https://www.usatoday.com/story/news/health/2022/07/28/marburg-virus-disease-outbreak-symptoms-treatment/10173445002/

The WHO calls the disease "epidemic-prone," meaning that it can spread easily between people if not prevented.

https://www.healthline.com/health-news/could-the-marburg-virus-start-another-outbreak-what-we-know

Marburg virus disease is a highly virulent disease that causes haemorrhagic fever, with a fatality ratio of up to 88%. It is in the same family as the virus that causes Ebola virus disease.

https://www.who.int/health-topics/marburg-virus-disease#tab=tab_1

Although MVD is uncommon, MARV has the potential to cause epidemics with significant case fatality rates.

https://www.ecdc.europa.eu/en/infectious-disease-topics/z-disease-list/ebola-virus-disease/facts/factsheet-about-marburg-virus

However, looking into the Marburg "virus" outbreaks tells an entirely different story. This is only the second reported outbreak of the Marburg "virus" in West Africa, a place where it was unheard of before. The first appearance in this region of what is considered a highly contagious "virus" said to spread through contact with bodily fluids was a single case reported in Guinea last year. Similar to the recent monkeypox outbreak, the patients diagnosed with Marburg in Ghana had no relation to each other, no travel history to an endemic country, nor any contact with any animals said to carry the "virus." Both were farmers who reported non-specific symptoms such as diarrhea, fever, nausea and vomiting. Sadly, they both succumbed to their symptoms after treatment at the hospital. The final toll of this outbreak of the "highly contagious virus" was limited to four people.

How did a "highly contagious virus," which has never been seen in West Africa before, make its way to that part of the continent when those infected had no history of travel to an area where the "virus" is said to be endemic? How did this deadly "virus" only infect one person in Guinea in 2021 and only 4 in Ghana in 2022 if it is highly virulent and contagious? In fact, in the vast majority of its history, the Marburg "virus" has shown that it is anything but "highly contagious," with the highest outbreak occurring in Angola in 2004 with only 252 cases. If we are to go by the CDC's own data, there have only been 475 total cases of this "highly contagious virus" worldwide since its discovery in 1967. Those statistics do not seem to jibe with the definition of a "epidemic-prone highly contagious, highly virulent virus."

So what is the story behind the Marburg "virus?" When and how did this dangerous pathogen burst onto the scene? What new symptoms of disease originally prompted the search for a novel etiological agent? What methods, if any, were employed in order to purify, isolate, and characterize the particles assumed to be the "virus?" Let's see what we can uncover about the first "virus" discovered in the Filoviridae family.

According to the CDC, the Marburg "virus," was discovered in 1967 after an outbreak of symptoms commonly associated with hemorrhagic fever occurred among laboratory workers conducting research who had come in contact with African green monkeys. It is one of seven species of "filovirus," with the other six belonging to separate versions of the Ebola "virus." The symptoms of the disease associated with the Marburg "virus" are non-specific and overlap with many different diseases, such as malaria, typhoid fever, or dengue and/or any of the "viral" hemorrhagic fevers that may be endemic to a specific area. This obviously makes clinical diagnosis difficult (i.e. impossible) due to the similarities between the diseases. In other words, there is nothing new nor specific regarding the Marburg "virus" as it is just another in a long chain of names given to the same symptoms of disease:

"Marburg virus disease (MVD) is a rare but severe hemorrhagic fever which affects both people and non-human primates. MVD is caused by the Marburg virus, a genetically unique zoonotic (or, animal-borne) RNA virus of the filovirus family. The six species of Ebola virus are the only other known members of the filovirus family.

Marburg virus was first recognized in 1967, when outbreaks of hemorrhagic fever occurred simultaneously in laboratories in Marburg and Frankfurt, Germany and in Belgrade, Yugoslavia (now Serbia). Thirty-one people became ill, initially laboratory workers followed by several medical personnel and family members who had cared for them. Seven deaths were reported. The first people infected had been exposed to Ugandan imported African green monkeys or their tissues while conducting research. One additional case was diagnosed retrospectively."

"Clinical diagnosis of Marburg virus disease (MVD) can be difficult. Many of the signs and symptoms of MVD are similar to other infectious diseases (such as malaria, typhoid fever, or dengue) or viral hemorrhagic fevers that may be endemic in the area (such as Lassa fever or Ebola). This is especially true if only a single case is involved."

https://www.cdc.gov/vhf/marburg/index.html

We can learn a lot about the "discovery" of this new "filovirus" from the writings of Werner Slenczka, a man who self-identifies as an expert in "filoviruses" as he was intimately involved with their origin. Dr. Slenczka is an associate professor at the Institute of Virology who helped identify the filament-like particles claimed to be the "virus" by way of electron microscopy. He wrote a few papers detailing what occured throughout the "discovery" process and offered some rather interesting revelations.

The first excerpts presented here are from a paper he published on the Marburg "virus" in 2007, 40 years after it was first identified. According to Slenczka, the first people "infected" with the "virus" in August of 1967 were treated in their own homes for up to 10 days. The symptoms were not alarming at first but progressively became worse as undisclosed treatments were administered. It was initially thought that the patients were suffering from typhoid fever or dysentery. As the symptoms became worse, the patients were admitted to the hospital. Of the 7 patients who became hemorrhagic, 5 eventually succumbed to their illness, some as soon as one day after admission. Cases of the new "virus" as well as estimates for the incubation period were eventually determined retrospectively. Interestingly, one of the patients with severe illness who was never hospitalized recovered completely on his own. Contrary to the claims of the mainstream media today, it was eventually decided at the time that the "virus" was not highly contagious as there were only a few secondary cases, no tertiary infections, and no new cases after the initial "outbreak."

In mid-September of 1967, experiments with Guinea pigs were started in order to determine the cause of the disease. The researchers serially passaged toxic goo between the Guinea pigs and created "similar" symptoms to the human disease after later passages, thus concluding that they had obtained a filterable "virus," even though they were unable to obtain any electron microscopy images of the "virus." Guinea pig spleen and liver tissues were examined by Slenczka using indirect fluorescence antibody testing and it was found that there were intracytoplasmic intrusions in the Guinea pigs, but not the humans. This method was used to select the blood of the "infected" animals which were then used for electron microscopy examination using a newly developed technique by the lead researcher. They subsequently "discovered" the "virus" in the animals (but not the humans) in November of 1967, nearly 3 months after the initial cases of the disease:

Forty Years of Marburg Virus 

"In early August 1967, patients with unusual symptoms indicating an infectious disease were admitted to the university hospitals in Marburg and Frankfurt. The first patients were treated in their homes for up to 10 days, even though the illness was described as beginning suddenly with extreme malaise, myalgia, headache, and a rapid increase in temperature to as high as 39°C or more. Although the clinical symptoms were not very alarming during the first 3–4 days, additional symptoms and signs appeared at the end of the first week. Gastrointestinal symptoms, such as nausea, vomiting, and diarrhea, indicated to health care practitioners that the diagnosis might be dysentery or typhoid fever. The patients were therefore admitted to a hospital. At admission, most patients were observed to have conjunctivitis, exanthema, and enanthema, but shigellae or salmonellae were not found. During the second week after onset of disease, patient temperatures fell to 38°C, and petechiae and more-severe signs of hemorrhagic diathesis were recorded for ∼25% of patients. As indicated by transaminase levels, liver destruction reached its maximum at days 7 and 8 after onset of disease. Leukopenia with the appearance of immature polymorphonuclear leukocytes and thrombocytopenia (<10,000 cells/mm3) were detected. Patients were bleeding from all body orifices and from needle punctures. When the outcome was fatal, death occurred during the second week after onset of disease, at day 9 on average (range, day 7–16). In some cases, patients died from severe hemorrhagic shock on the day after hospital admission. Severe hemorrhagic signs, as seen in ∼25% of patients, were a signum mali ominis. All patients who died had hemorrhaging. Of 7 patients with manifest hemorrhages, 5 succumbed to the disease. Orchitis, a typical late-stage symptom, appeared in the third week after onset of disease or even at relapse during the fifth week. Mental confusion and paraesthesias were indicative of cerebral involvement. Relapses with hepatitis, orchitis, and uveitis with virus persisting in semen and in the anterior eye chamber were typical during the convalescent phase of both Marburg virus (MARV) and Ebola virus (EBOV) infections. In 1 case, a patient transmitted infection to his wife 120 days after onset of his disease, most probably by sexual intercourse. Virus was detectable in seminal fluid.

The incubation time of MARV disease could only be estimated retrospectively, after the source of infection and the date of exposure were known. Incubation ranged from 5 to 9 days, with an average of 8 days. The ratio of primary to secondary infections was 21:3 in Marburg, 4:2 in Frankfurt, and 1:1 in Belgrade. Three cases of secondary infection resulted from inadvertent needle-stick inoculations; in 1 case, a pathology technician cut himself on the forearm with a knife during a postmortem examination. Airborne transmission between humans did not occur, as indicated, for example, by the instance of a young man who slept in the same bed with his brother only a couple of days before he died; the brother did not develop disease and was seronegative for MARV 6 months later. One of the patients had been severely ill at the time of the outbreak but, for unknown reasons, was not hospitalized. He recovered and, 15 years later, maintained that he had had MARV disease. At that time, he underwent serological testing and was found to be seropositive for MARV antibody by IFA and ELISA. He had been exposed to monkey kidney cell cultures, which were used for the production of poliomyelitis vaccine. At 6 months after the outbreak, blood specimens were obtained from 120 persons who had been in close contact with patients or with infectious material but who had not developed disease. The specimens were tested for MARV antibody by complement fixation test, IFA, and ELISA and were found to be seronegative. Therefore, there was no indication of clinically inapparent infection."

"By mid September, it had become evident that the agent exhibited a low contagiousness. Only a few cases of secondary infection and no cases of tertiary infection had occurred, and no new cases had occurred during the previous 2 weeks. Therefore, Rudolf Siegert (figure 1) resumed experiments with guinea pigs, together with a Chinese colleague, Hsin Lu Shu. They found that the agent could be passed among guinea pigs and exhibited pathogenicity that increased from passage to passage. At the third passage, the animals fell ill with fever, hepatitis, and hemorrhagic disease that closely resembled human disease, and they died within 10 days after inoculation, with a marked drop in temperature. However, all efforts to determine the etiological agent by light or electron microscopy failed. Opportunistic bacterial infections were a major problem.

At this time, specimens of human and guinea pig convalescent serum were available, and some of the serum specimens were tagged with fluorescein for direct IFA. Three weeks later, W.S. (figure 1) detected intracytoplasmic inclusions in the tissues of infected guinea pigs, by IFA. Animals that had infected cells in the liver and spleen were selected for further studies using electronmicroscopy. Blood specimens from these animals were inactivated with formalin and sent to Dietrich Peters at the Bernhard Nocht Institute in Hamburg. Formalinized plasma was spun directly onto electron microscope (EM) grids, by means of a new technique developed by Gerhard Müller, and negative staining was done. By these methods, MARV was identified on 20 November, < 3 months after the outbreak had begun (figure 2)."

https://academic.oup.com/jid/article/196/Supplement_2/S131/858753

It needs to be noted that, according to Slenczka's account of the events, no "virus" was ever properly purified and isolated at any point during the investigation into the potential cause of disease afflicting the laboratory workers in 1967. In fact, the initial evidence for the existence of the Marburg "virus" essentially boiled down to experimentally making Guinea pigs sick through serial passaging of unnatural injections of blood/tissues into their stomachs, examining their spleens and livers using non-specific antibodies to find non-specific inclusions, and then taking electron microscopy images of the sickened animals blood and claiming random particles seen in the unpurified and contaminated samples are the "virus" in question. Eventually, after many unsuccessful attempts of trial and error failures, it was claimed that the "virus" could be propagated in cell culture (without CPE) using the Guinea pig (not human) materials.

For a better understanding of the fraudulent methods used to propagandize the public on a new deadly "virus," let's break down the main three focus areas (animal experiments, EM imaging, and cell culture) even further and see what the evidence shows.

1. Animal Experimentation

"Experimental infection apparently results in 100% fatality. If this situation occurs in nature, obviously there could not be any serologic positives. However, if the experimental route of inoculation differs from that occurring in nature, it is possible that 100% fatality will not develop."

https://link.springer.com/chapter/10.1007/978-3-662-01593-3_22

The first piece of evidence used for the existence of a new "virus" was the creation of "similar" symptoms in Guinea pigs by continually injecting them with serially passaged diseased fluids/tissues. What these injections actually contained is difficult to determine as the original study is in German and the translation is not clear. The study, lead by Rudolf Siegert, mentioned doing successive passages with whole blood, plasma or organ material yet what the exact methods were beyond that remain obscure due to a faulty translation.

Fortunately Rudolf Siegert collected much of the Marburg research into a book in 1971. Oddly, he did not include his original paper On the etiology of an unknown human infection originating from monkeys yet he did provide a study explaining the procedures used for passaging the "virus" in Guinea pigs which furnished some insight into the kind of experiments that were ultimately carried out. What we can see in the highlights from the included paper below is that the clotted blood was haemolyzed with sterile distilled water and the organs triturated using a cold mortar. A phosphate buffer diluent containing 10 p. 100 normal rabbit serum was added to the blood mixture which was used to inject mice intracerebrally (in the brain) and intraperitoneally (in the stomach) as well as Guinea pigs intraperitoneally. The researchers admitted that all "isolation" attempts were negative except for in Guinea pigs as, after injecting the Guinea pigs in the stomach with blood samples, organ suspensions, and Cercopithecus organ pools, the animals developed a febrile (fever) reaction 4 to 6 days after inoculation. Clinical symptoms in the animals included loss of appetite and weight, "bloated face," and enlargement of the testes. The researchers concluded that from the human and monkey material, an organism was "isolated" and transmitted through four to six passages in Guinea pigs even though no "virus" was ever purified, isolated, and visualized:

Passage of Marburg Virus in Guinea Pigs

"Clotted blood was haemolyzed with sterile distilled water and the organs triturated using a cold mortar and phosphate buffer diluent containing 10 p. 100 normal rabbit serum added to give a final concentration of about 20 percent by volume."

"Suckling mice were inoculated intracerebrally (ic) and intraperitoneally (ip) with 0.02 ml.

Guinea pigs (200-300 g) were inoculated ip with 4 ml. For further passaging, whole blood harvested by cardiac puncture was injected ip."

Results

All isolations attempts have been negative except in guinea pig. 

Guinea pig Passages 

Guinea pigs injected by ip route with blood samples of patient H. F. (HF 1 and HF 2) organ suspensions of patient P. S. and Cercopithecus organ pools M 10 and M 14 consistently developed a febrile reaction 4 to 6 days after inoculation. 
The febrile stage lasted 3 to 7 days. 

Whole blood taken during this febrile stage has been successfully passaged ip in guinea pigs through 3 to 6 passages (Figs. 1 to 5). The incubation period was shortened to 2-3 days and some guinea pigs died from 7 to 17 days after inoculation. Clinical symptoms in the animals were: loss of appetite and weight, "bloated face" and enlargement of the testes. At autopsy, we found splenomegaly and lung consolidation. 

Fever reactions in guinea pigs were produced using early blood samples from the preceding passage. In one instance (Fig. 4, passage 4), fever reaction followed inoculation of blood taken at the 11th day. This fact confirms observation that infection seems to produce a long lasting viraemia."

Conclusions 

"The results reported above show that from human and monkey material, an organism has been isolated and transmitted through four to six passages in guinea pigs."

DOI: 10.1007/978-3-662-01593-3_16

As can be seen from the above study, the researchers are conflating the experimental creation of disease in Guinea pigs through serial passaging and unnatural routes of infection with the "isolation" of a "virus." At no point was a "virus" ever purified and isolated from the fluids of a sick human, a monkey, nor a Guinea pig. Beyond the non-specific fever, weight loss, and loss of appetite (occuring after injections of toxic unpurified goo into the stomach), none of the symptoms experienced by the Guinea pigs (bloated face, enlarged testes) related to the human condition whatsoever. In fact, Rudolf Siegert and Werner Slenczka later admitted in their paper Laboratory Diagnosis and Pathogenesis, that regarding the pathogenesis of the disease in man, "apparently the virulence of
the Marburg virus differs in monkey, man, and guinea pig." Yet it was based on these experimental results that it was determined a new pathogenic "virus" was hiding in the fluids of the sickened Guinea pigs which were then used for electron microscopy imaging in order to try and find the new "virus."

2. Electron Microscopy Images

The second possibility of making a rapid diagnosis lies in the direct demonstration of the virus with the electron microscope. This may succeed if the agent is directly centrifuged from serum or plasma on a carrier, according to Peters and Muller [7]. The characteristic morphology leaves no doubt as to the diagnosis. However, we have no experience enabling us to answer the question concerning
the probability that the agent may be overlooked with this method. It is for this reason that attempts to isolate the virus in guinea pigs and in various cell culture systems should follow in any case.

https://link.springer.com/chapter/10.1007/978-3-662-01593-3_22

While the researchers failed in their initial attempts to identify the "virus" by electron microscopy after sickening the Guinea pigs, they eventually determined through direct and indirect antibody staining results that they could find the "virus" in the livers and spleens of these animals. While Rudolf Siegert's study did not offer much insight into how they determined that the particles observed were the actual "virus" they were looking for, he did offer some interesting comments about their morphology which fortunately were not lost in translation:

On the etiology of an unknown human infection originating from monkeys

"The results described show that "Marburg Virus" is not identical, but it is morphologically closely related to the virus vesicular stomatitis (1, 2, 6, 9, 11, 12), the Coval (1, 3) Egtved- (13) and finally the rabies virus (8, 10). A fundamental difference from these viruses seems to have the particular tendency to be growth in length."

DOI: 10.1055/s-0028-1106144

According to Seigert, the particles he observed looked morphologically like the vesicular stomatitis, coval, egtved, and rabies "viruses." The main difference was in the length of the particles. However, does the length of the particles really distinguish these "viruses" from each other all that much? Could these all be random pieces from the same long strands broken apart or even created from the procedures used to capture the images? Presented below are the images of the Marburg "virus" supplied by Seigert which show some longer particles mixed with other smaller particles which resemble the bullet shape of the aforementioned "viruses" listed in his paper. The third image included is one provided by Slenczka said to be from the original "isolate" in 1967 while the colorized pictures are images taken from recent 2022 articles on the Marburg "virus" cases in Ghana:

https://www.bmj.com/content/378/bmj.o1797
https://www.indiatoday.in/amp/information/story/what-is-marburg-virus-1977711-2022-07-20

As can be seen, the Marburg "virus" comes in different shapes and sizes, from long filament particles to smaller bullet-like particles to even those resembling "corona-like" structures. It seems that the image of the "virus" heavily depends upon the way the picture is taken/cropped as well as how the particles are stained and colorized. Below are images of the "viruses" said by Seigert to be morphologically similar to the Marburg "virus:"

Vesicular Stomatitis

In these images, we can see the similar bullet-like shape in the vesicular stomatitis "virus" as seen in the particles claimed to be the rabies "virus." Interestingly, the particles appear to vary in size from the smaller bullets to the much more elongated forms resembling the Marburg "virus." This "unwinding" was described in the third image as most likely a result of the negative staining procedures done to visualize the "virus" particles.

https://www.utmb.edu/virusimages/VI/vesicular-stomatitis-indiana-virus
https://www.nature.com/articles/ncomms2435
"The difference in degree of unwinding is probably caused by intrinsic variations in the negative staining procedure due to differences in local hydrophilicity of the support film, sample concentration, room temperature, and humidity." https://www.researchgate.net/figure/EM-of-VSV-structure-Negative-staining-was-done-with-I-N-SST-A-Intact-VSV-The_fig1_14969735
Viral Haemorrhagic Septicemia Virus (VHSV)

The VHSV is a fish "virus" that also supposedly shares the exact same shape as the rabies "virus" and is morphologically similar to the Marburg "virus." As can be seen, the shapes of the particles once again range from small bullet-like entities to longer filaments, perhaps caused once again by the negative staining procedures.

https://www.researchgate.net/publication/6080687_Mortality_event_in_freshwater_drum_Aplodinotus_grunniens_from_Lake_Ontario_Canada_associated_with_viral_haemorrhagic_septicemia_virus_Type_IV
https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/viral-hemorrhagic-septicemia-virus
https://www.adfg.alaska.gov/static/species/disease/pdfs/fishdiseases/north_american_viral_hemorrhagic_septicemia_virus.pdf
Rabies

Even the rabies "virus," said to be the bullet-like particles seen in the TEM images, show various shapes and sizes depending on the staining and colorization. Some appear to be long Marburg-like filament forms that happen to be present in a U-shape upon imaging. Interestingly enough, up to the early 1980's, the Marburg "virus" was classified as a rhabdovirus due to the similarities between the morphology of the "viruses." It was even originally given the moniker Rhabdovirus simiae.

https://www.cdc.gov/rabies/diagnosis/electron_microscopy.html
https://en.m.wikipedia.org/wiki/Rabies_virus
https://fineartamerica.com/featured/tem-of-rabies-viruses-cnriscience-photo-library.html

While it is easy to see the similarities between the Marburg "virus" and the other "viruses" Seigert highlighted in his study, he failed to mention that we can find similar looking filament particles associated with many other "viruses" as well:

Mumps
https://www.ecdc.europa.eu/en/immunisation-vaccines/facts/vaccine-preventable-diseases
https://www.virology.uct.ac.za/vir/teaching/linda-stannard/paramyxovirus
https://www.robertharding.com/index.php?lang=en&page=search&s=mononegavirales&smode=0&zoom=1&display=5&sortby=1&bgcolour=white
Measles
https://europepmc.org/articles/pmc375751?pdf=render
https://www.sciencephoto.com/media/248676/view/measles-virus-tem
Parainfluenza
https://www.alamy.com/stock-photo/human-parainfluenza-virus-hpiv.html
https://pharmaceutical-journal.com/article/news/existing-drugs-are-effective-against-human-parainfluenza-virus
https://www.sciencephoto.com/media/247979/view/coloured-tem-of-parainfluenza-virus-particles
https://www.sciencephoto.com/media/1010244/view

It can be seen that the images of these particles claimed by Seigert to be of different "viruses" definitely share similar morphology (i.e. form and structure). It is clear that the staining and colorization of the particles as well as how they are zoomed in and presented definitely influences how they appear in the images. It is even stated in one study that the negative staining procedures have an impact on how the particles form. It is evident, when including images of filament forms of other "viruses," that this is yet another case where the same particles (seen in various stages of formation/degradation) are being cropped from an unpurified sea of different shapes and structures and focused on as the representative culprit in numerous diseases.

As the electron microscopy images play such a pivotal role in the proof supplied for the Marburg "virus," it is important to gain some greater insight into the electron microscopy process used by Werner Slenczka and Co. in order to identify the Marburg "virus." For this we can now turn our attention to a 2017 article he wrote describing how his "filovirus" research began. In this account, we find out that the blood samples taken from the Guinea pigs were mixed with glutaraldehyde and formaldehyde before imaging. Slenczka admitted that searching for an unknown pathogenic agent in EM can be fatiguing and frustrating as he explained that many contaminants can be found within the sample. This was the case with the Marburg "virus" as numerous microbial contaminants were present in the sample (thus it was unpurified and not isolated) which made the interpretation of the data difficult. As stated before, the spleens and livers of the Guinea pigs were used for EM imaging utilizing direct and indirect antibody fluorescence, and the samples were air-dried and fixed with ice-cold acetone. Since they did not know if the unknown agent would be killed by acetone, Slenczka claimed that they handled the slides with extreme caution. It then took them 3 weeks of hard work to get the initial results. Slenczka stated that what he saw in his slides resembled the Negri bodies said to be specific to the rabies "virus" yet somehow this finding told him that this effect was the cause of a new "virus." He used his initial findings to mark any Guinea pig sample with these inclusions as ones with the "virus" in need of further analysis by EM.

The blood samples which were selected for further analysis were once again subjected to glutaraldehyde and formaldehyde and studied. Dr. D. Peters, along with his technician, spent more than a day looking through the samples with no results. On the second day, Dr. Peters left the search for a lunch break and handed the reigns to Dr. G. Müller. Once Dr. Peters arrived back from his lunch break, he was informed by Dr. Müller that the "virus" had been found (in less than an hour) as they had observed unknown particles of a different morphology and structure to any that had been seen before. Obviously, this is not the case as these same particles have been observed with various "viruses" as detailed previously. Ultimately, the entire "isolation" process did not involve the purification and isolation of any "virus" directly from human fluids and instead relied entirely on assumptions based on indirect evidence obtained from animal, antigen, and EM studies using unpurified and non-isolated material from Guinea pigs rather than humans.

Interestingly, as the laboratory researchers who were initially "infected" with the "virus" were conducting polio vaccine research using monkey kidney cell cultures, it was assumed that the "virus" came from the imported monkeys. However, according to Slenczka, none of the monkeys at any of the laboratories ever showed any signs of disease at any location. He also stated that the exact lethality data of the incriminated monkeys was never communicated. Thus, it was left up to mere assumptions that some persistently infected monkeys from "Monkey island" which were caged for research may have been the source for importing Marburg "virus" to Europe. According to Slenczka, it was known that a large number of monkeys from the same source in Uganda were transported to Sweden, Japan, Czechoslovakia, Italy, Switzerland, and England at the same time for the purpose of preparing cell cultures. However, no outbreaks were reported at any of these locations. Thus, Slenczka was forced to admit that his hypothesis, just like his "virus," was solely based on assumptions:

Filovirus Research: How it Began

"These experiments were a step in the right direction, but the agent remained unidentified. To facilitate identification, blood from infected animals, taken at the climax of the disease, was mixed with glutaraldehyde and formaldehyde to inactivate and preserve the unknown agent and was sent to the electron microscopy (EM) laboratories at the University of Marburg and the Bernhard Nocht Institute for Tropical Medicine in Hamburg, Germany for analysis: Dr. D. Peters, head of the
Virology Department at the Bernhard Nocht Institute, was a renowned virological electron microscopist and highly experienced in analyzing viral structures.

Of course, EM-based search for an unknown pathogen in biological materials can be extremely fatiguing and––in case of a negative result––very frustrating.

In the case of the guinea pig material, an additional obstacle became evident soon. A serious complication, often encountered in the search for unknown pathogens, is contamination by organisms unrelated to the disease. These "pick-up" contaminants may interfere with the etiological agent or may even cause disease themselves. Contamination may occur as a result of a preexisting infection. During passage to new animals, contaminants might be transferred with a higher efficiency than the unknown etiological agent. The risk of cultivating a contaminating agent may be reduced by using animals from an SPF (specific pathogen free) breed. In 1967, SPF guinea pigs could not be afforded in Marburg. Instead, the animals were purchased from local breeding stations which did not control for infections. Therefore, in the experiments carried out by Drs. Siegert and Shu, it happened that microbial contaminations, including pseudomonads, pasteurellae, and in some cases paramyxoviruses were present in the guinea pigs. Although it was quite clear that these well-known organisms were not the etiological pathogen, the presence of these contaminants complicated data interpretation."

"Organs from infected and noninfected guinea pigs, especially livers and spleens, were used to make imprint preparations on microscopic slides, which were then air-dried and fixed with ice-cold acetone. Since we did not know if the unknown agent would be killed by acetone, we handled these slides with extreme caution. It took 3 weeks of hard work before we had the first results. I found brilliantly fluorescent cytoplasmic inclusions in liver cells from an infected guinea pig. Since all the controls were negative, I was sure I had found antigenic structures of the unknown pathogen (Fig. 4). At this time, it was not yet possible to tell whether these inclusions, which resembled the Negri bodies found in rabies virus-infected cells (Goldwasser et al. 1959), were indicative of a viral or bacterial infection. However, it was clear that I had detected something that nobody had seen before; structures of an unknown agent causing a deadly disease (Slenczka et al. 1968).

Using this assay, it was now possible to identify those animals which were infected with this agent to select material for EM investigations. Once again, guinea pig blood treated with glutaraldehyde and formaldehyde was sent to the Bernhard Nocht Institute in Hamburg for EM analysis. Dr. D. Peters, together with a technician, analyzed negative stained material for more than a day but did not observe anything reminiscent of a viral structure. On the second day of his search, Dr. Peters left the laboratory for a lunch break and handed the specimen to his coworker, Dr. G. Müller, asking him to continue the search. In less than an hour, Dr. Müller had succeeded in finding viral particles that, due to their sizes and unique morphologies, were identified as the products of an unknown virus (Fig. 5). When Dr. Peters returned from his lunch break, Müller showed him the new virus. It is not clear why Dr. Peters had not found the viral particles when he examined the samples. The most probable explanation seems to be that the particles had spontaneously sedimented to the bottom of the tube and Dr. Peters took material from the top only."

"The researchers who deserve credit for isolating and identifying Marburg virus are Walter Mannheim, University of Marburg for successful transmission to guinea pigs, Werner Slenczka, University of Marburg for detecting and identifying the Marburg virus antigen by immunofluorescence analysis, and Gerhard Müller, Bernhard Nocht Institute for identifying the virus by EM. Walter Mannheim, a bacteriologist, was uninterested in co-authoring publications despite his involvement in the virus isolation."

"The most intriguing question regarding these monkeys is their state of health. Where and at what time did they acquire the virus? Why did they not show signs of disease at any location; not when they were in Entebbe, not upon their arrival in London, Frankfurt, Marburg, or Belgrade, and not when they were finally euthanized? The lethality of imported NHPs was about 5% at that time. An increase in lethality of imported NHPs should certainly have raised suspicion. Exact lethality data of the incriminated monkeys were never communicated. There can be no doubt that the animals were inspected carefully before they were used."

"Assuming that some persistently infected monkeys from "Monkey island" could have been the source for importing Marburg virus to Europe might help to explain some peculiarities of this outbreak. It is known that a large number of monkeys from the same source in Uganda were transported to Sweden, Japan, Czechoslovakia, Italy, Switzerland, and England at the same time and for the same purpose: to prepare cell cultures. But no outbreaks were reported at any of these locations. It is possible that when the shipments to Germany and to Yugoslavia were assembled, there were not enough monkeys left at the collecting station and therefore, that animals from "Monkey island" were used to supplement the shipment. Among the animals captured from "Monkey island" were possibly some which had survived an infection with Marburg virus but appeared to be healthy. This might explain why Marburg virus was exclusively transported with shipments to locations in Germany and in Yugoslavia.

Admittedly, the above-formulated hypothesis is based on assumptions. But it offers an intriguing explanation addressing many of the open questions regarding this outbreak that, until now, have remained unanswered."

https://pubmed.ncbi.nlm.nih.gov/28766193/

3. Cell Culture

In cell cultures cytopathic alterations are absent. However, as early as the
third day cytoplasmic antigen inclusions may be recognized, which increase considerably in number and size until the 7th day.

https://link.springer.com/chapter/10.1007/978-3-662-01593-3_22

Beyond the issues related to the interpretation of contaminated and unpurified EM images and the lack of disease in the monkeys assumed to have been carriers of the "virus," early attempts to propagate the "virus" in cell cultures failed miserably. Many different cell lines were used and conflicting results were often obtained. Many times, the researchers claimed that the "virus" successfully replicated in the cells even though the required cytopathogenic effect (CPE) was never observed. This is the effect which virologists use to claim that the structural changes observed in a host cell during culturing are the result from "viral" infection and replication. As one source stated, the CPE is a way of "seeing" and indirectly measuring a "viral" infection by looking at the damage a "virus" causes to a cell. This damage is a measurement that is widely used in virology labs all over the world in order to determine indirectly the presence of a "virus." Without observing such an effect, the culture should theoretically show that no "virus" is present in the sample. However, as this effect is not always observed, virologists found a way around the lack of being able to produce this effect in all cultures by claiming that some "viruses" do not produce CPE at all while others only do so in certain cell lines. They state that even without the observance of CPE, the cultures are still successful despite the lack of any structural changes denoting the highjacking of the cell by the "virus" and the subsequent replication process.

The below highlights are from a 1971 paper which summarized the attempts to cultivate the Marburg "virus" and explained the confusing and contradictory results. The authors concluded that while the "virus" could be propagated in culture, the general rule was that no gross cytopathic changes could be observed:

Cultivation of the Marburg Virus (Rhabdovirus simiae) in Cell Cultures

"At the time when the causative agent of Marburg haemorrhagic fever was still unknown, attempts were made to isolate the agent from patients. For isolation purposes laboratory animals and many cell systems were employed but all initial trials in cell cultures were unsuccessful (SIEGERT et aI., 1967; MAY and KNOTHE,1968; SIEGERT et aI., 1968). Later when the virus was isolated in guinea pigs (SIEGERT et aI., 1967; SMITH et aI., 1967; KUNZ et aI., 1968; MAY and KNOTHE, 1968; KISSLING et aI., 1968), many investigators tried to propagate Marburg virus in various cell cultures. Presently, much data are available which will be summarized in this report."

In primary cells of Cercopithecus kidney, the species with which the agent was imported to Germany, SIEGERT et aI. (1968) found that the virus replicated without cytopathic effect (CPE). They also demonstrated the virus specific antigen by means of the immunofluorescent method. On the contrary HAAS et aI. (1968) observed gross CPE in primary Cercopithecus kidney cells. These cells were only less sensitive to the virus than subcutaneously infected Cercopithecus monkeys.

In primary Rhesus monkey kidney cells, the virus replicated but without CPE (HOFMANN and KUNZ, 1968). Primary cells of human origin also propagated the virus. MAY and KNOTHE (1968) could not observe CPE in human leucocytes but reported slight CPE in primary human amnion cells (MAY et aI., 1968).

We could demonstrate replication of the virus in primary guinea pig embryo fibroblasts but no CPE was seen (HOFMANN and KUNZ, 1968).

In chick embryo cells, we found a very slight virus replication (HOFMANN and KUNZ, 1968), while other investigators did not observe propagation at all (SMITH
et aI., 1967; MAY and KNOTHE, 1968)."

"Established cell lines were also investigated for propagation of Marburg virus. At first cells derived from monkeys were tested. Although we found that permanent Cercopithecus kidney cells (strain GMK-AHl) produced high titers of virus-1 ml of culture fluid contained 10^6 infective doses for guinea pigs-we could not demonstrate any CPE. KISSLING et aI. (1968) were more successful; they observed CPE in their cultures in the second day p.i., which was in total about the 4th-5th day.

In the VERO cell line, the virus also propagated. No CPE was observed by SIEGERT et aI. (1968) and only slight CPE by KISSLING et aI. (1968).

From cells of Rhesus monkey origin, heart cells (strain CMH) allowed only slight virus growth (HOFMANN and KUNZ, 1968), while in kidney cells (strain LLC-MK2) no virus replication was demonstrable (SMITH et aI., 1967).

In the studies of SMITH et aI. (1967) the Marburg virus propagated in L cells (mouse embryo cells) without CPE; we could not demonstrate any virus growth in those cells.

Heart cells derived from guinea pigs also allowed virus replication without CPE (KISSLING et aI., 1968).

The first reports of Marburg virus-induced CPE in cell cultures were by ZLOTNIK et aI. (1968). They had found that the virus was adaptable to BHK21 cells. In the first passage typical inclusion bodies similar to those found in guinea pig liver, were seen in infected cells after 13 days and CPE appeared about the 23rd day. After a few passages, inclusion bodies as well as CPE appeared earlier. In our laboratory BHK21 cultures showed only slight changes which appeared very late (HOFMANN and KUNZ, 1968). KISSLING et aI. (1968) tested two strains of BHK21 . One, the WI 2 strain, behaved as the strain in our laboratory, but the other was highly susceptible. Cytopathic effect was observed about the 2nd-5th day after infection.

In contrast to 3 other teams of investigators (SIEGERT et aI., 1968; SMITH et aI., 1967; MAY and KNOTHE, 1968), we could propagate Marburg virus quite well in our HeLa strain. One ml of culture fluid contained 104 infective particles for guinea pigs, however we found no CPE (HOFMANN and KUNZ, 1968).

Other strains deriving from human sources were also tested for Marburg virus induced CPE. KISSLING et aI. (1968) propagated the virus in foreskin fibroblastsIn the first passage of virus CPE was demonstrable but could not be reproduced in serial passages. In U cells, a stable cell line of human amnion, the agent also replicated but without CPE (HOFMANN and KUNZ, unpublished).

In our laboratory we had previously tested many cell systems, but we were unable to detect a cell line in which Marburg virus propagates with CPE. Finally we came across the ELF (embryonal human lung fibroblasts) cell strain, in which CPE appears about the 3rd day and reaches its maximum about the 5th day after infection. Cytopathic effect begins in focal areas and consists of spindling and later on of clumping of cells. Finally the foci become confluent (see Figs. 1-3). It must be mentioned that, although changes are severe, they are never complete and eventually healthy cells may grow in and repair the lesions."

"Summarizing the sometimes conflicting results obtained by the various investigators, it can be stated that cells deriving from mammals such as monkey, guinea pig, and hamster and human cells are susceptible to the virus. Often high titers were produced by the cells although as a rule no gross cytopathic changes could be observed."

https://link.springer.com/chapter/10.1007/978-3-662-01593-3_15

Fear Propaganda #1
In Summary:
  • Marburg "virus" disease (MVD) is said to be a rare but severe hemorrhagic fever which affects both people and non-human primates
  • It is one of seven belonging to the Filoviridae group, with the other six species of Ebola "virus" the only other known members of the "filovirus" family
  • Marburg "virus" was first recognized in 1967, when outbreaks of hemorrhagic fever occurred simultaneously in laboratories in Marburg and Frankfurt, Germany and in Belgrade, Yugoslavia (now Serbia)
  • The first people "infected" had been exposed to Ugandan imported African green monkeys or their tissues while conducting research
  • Clinical diagnosis of Marburg "virus" disease (MVD) can be difficult as many of the signs and symptoms of MVD are similar to other infectious diseases (such as malaria, typhoid fever, or dengue) or "viral" hemorrhagic fevers that may be endemic in the area (such as Lassa fever or Ebola)
  • The first patients were treated in their homes for up to 10 days, even though the illness was described as beginning suddenly with extreme malaise, myalgia, headache, and a rapid increase in temperature to as high as 39°C or more
  • Although the clinical symptoms were not very alarming during the first 3–4 days, additional symptoms and signs appeared at the end of the first week
  • Gastrointestinal symptoms, such as nausea, vomiting, and diarrhea, indicated to health care practitioners that the diagnosis might be dysentery or typhoid fever
  • In some cases, patients died from severe hemorrhagic shock on the day after hospital admission
  • Note that there is zero information on what treatments the patients underwent before and after admission to the hospital which could have worsened their clinical symptoms
  • Airborne transmission between humans did not occur, as indicated, for example, by the instance of a young man who slept in the same bed with his brother only a couple of days before he died; the brother did not develop disease and was seronegative for MARV 6 months later
  • One of the patients had been severely ill at the time of the outbreak but, for unknown reasons, was not hospitalized and recovered and, 15 years later, maintained that he had had MARV disease (full recovery from severe illness without hospital admission/treatment… 🤔)
  • By mid September, it had become evident that the agent exhibited a low contagiousness
  • Only a few cases of secondary infection and no cases of tertiary infection had occurred, and no new cases had occurred during the previous 2 weeks
  • Rudolf Siegert performed experiments with Guinea pigs and found that the agent could be passed among Guinea pigs and exhibited pathogenicity that increased from passage to passage (i.e. the more they injected Guinea pigs with cultured diseased goo and tissues, the more they became sick)
  • However, all efforts to determine the etiological agent by light or electron microscopy failed and opportunistic bacterial infections were a major problem
  • In other words, they claimed there was a "virus" inside the toxic goo serially passaged and injected into Guinea pigs but they could not find it
  • After this failure, specimens of human and Guinea pig convalescent serum were available, and some of the serum specimens were tagged with fluorescein for direct IFA
  • Three weeks later, W.S. detected intracytoplasmic inclusions in the tissues of infected guinea pigs, by IFA
  • Formalinized plasma was spun directly onto electron microscope (EM) grids, by means of a new technique developed by Gerhard Müller, and negative staining was done
  • By these methods, the Marburg "virus" was identified on November 20, 1967, almost 3 months after the outbreak had begun
  • For the Guinea pig experiments, clotted blood was haemolyzed with sterile distilled water and the organs triturated using a cold mortar and phosphate buffer diluent containing 10 p. 100 normal rabbit serum added to give a final concentration of about 20 percent by volume
  • Suckling mice were inoculated intracerebrally (IC) and intraperitoneally (IP) with 0.02 ml while Guinea pigs (200-300 g) were inoculated IP with 4 ml
  • For further passaging, whole blood harvested by cardiac puncture was injected IP
  • All isolations attempts were negative except in Guinea pigs
  • Guinea pigs injected by IP route with blood samples of patient H. F. (HF 1 and HF 2) organ suspensions of patient P. S. and Cercopithecus organ pools M 10 and M 14 consistently developed a febrile reaction (i.e. fever) 4 to 6 days after inoculation
  • Whole blood taken during this febrile stage had been successfully passaged IP in Guinea pigs through 3 to 6 passages
  • The incubation period was shortened to 2-3 days and some Guinea pigs died from 7 to 17 days after inoculation
  • Clinical symptoms in the animals were:
    1. Loss of appetite and weight
    2. "Bloated face"
    3. Enlargement of the testes
  • The researchers felt that the results reported showed that from human and monkey material, an  organism had been "isolated" and transmitted through four to six passages in Guinea pigs
  • In other words, injecting diseased tissues and fluids successively into Guinea pigs and causing symptoms equalled "isolating a virus"
  • According to the electron microscopy imaging search for the "virus," Rudolf Siegert described the particles seen as morphologically closely related to the vesicular stomatitis "virus," the Coval, Egtved, and the rabies "virus"
  • A fundamental difference from these "viruses" seemed to have the particular tendency to grow in length
  • In order to identify the "virus" particles in EM, blood from infected animals, taken at the climax of the disease, was mixed with glutaraldehyde and formaldehyde to inactivate and preserve the unknown agent
  • Werner Slenczka admitted that EM-based search for an unknown pathogen in biological materials can be extremely fatiguing (which would not be the case in a purified/isolated preparation)
  • A serious complication, often encountered in the search for unknown pathogens, is contamination by organisms unrelated to the disease
  • These "pick-up" contaminants may interfere with the etiological agent or may even cause disease themselves
  • During passage to new animals, contaminants might be transferred with a higher efficiency than the unknown etiological agent
  • In 1967, special pathogen-free  guinea pigs could not be afforded in Marburg so the animals were purchased from local breeding stations which did not control for infections
  • Therefore, in the experiments carried out by Drs. Siegert and Shu, it happened that microbial contaminations, including pseudomonads, pasteurellae, and in some cases "paramyxoviruses" were present in the guinea pigs
  • The presence of these contaminants complicated data interpretation
  • Samples were air-dried and fixed with ice-cold acetone yet, as they did not know if the unknown agent would be killed by acetone, they handled these slides with extreme caution
  • It took 3 weeks of hard work before they had the first results
  • Slenczka found inclusions within the samples which resembled the Negri bodies found in rabies "virus-infected" cells
  • Somehow, finding the same inclusions as seen in rabies led Slenczka to believe that this was the result of a new "virus"
  • Dr. D. Peters, together with a technician, analyzed negative stained material for more than a day but did not observe anything reminiscent of a "viral" structure
  • On the second day of his search, Dr. Peters left the laboratory for a lunch break and handed the specimen to his coworker, Dr. G. Müller, asking him to continue the search and in less than an hour, Dr. Müller had succeeded in finding "viral" particles that, due to their sizes and unique morphologies, were identified as the products of an unknown "virus"
  • Remember that it was admitted that the Marburg "virus" resembled many other "viruses," including rabies, morphologically
  • It is not clear why Dr. Peters had not found the "viral" particles when he examined the samples
  • According to Slenczka, the researchers who deserve credit for "isolating" and identifying Marburg "virus" are:
    1. Walter Mannheim, University of Marburg for successful transmission to guinea pigs (he was uninterested in co-authoring publications despite his involvement in the "virus" isolation)
    2. Werner Slenczka, University of Marburg for detecting and identifying the Marburg "virus" antigen by immunofluorescence analysis
    3. Gerhard Müller, Bernhard Nocht Institute for identifying the "virus" by EM
  • Note that the entire "isolation" process did not involve the purification and isolation of any "virus" directly from human fluids and instead relied entirely on assumptions based on indirect evidence obtained from animal, antigen, and EM studies using unpurified and non-isolated material from Guinea pigs
  • As the laboratory workers who were sickened were working on polio research using monkey kidney cell cultures, it was assumed that they had become infected from the imported monkeys
  • However, none of the monkeys showed signs of disease at any location
  • Exact lethality data of the incriminated monkeys was never communicated
  • Slenczka assumed that some persistently infected monkeys from "Monkey island" could have been the source for importing Marburg "virus" to Europe
  • It was known that a large number of monkeys from the same source in Uganda were transported to Sweden, Japan, Czechoslovakia, Italy, Switzerland, and England at the same time and for the same purpose: to prepare cell cultures
  • However, no outbreaks were reported at any of these locations
  • Slenczka admitted that his formulated hypothesis was based on assumptions
  • As stated before, the attempts to isolate a "virus" from human patients failed
  • For isolation purposes laboratory animals and many cell systems were employed but all initial trials in cell cultures were unsuccessful
  • It wasn't until when the "virus" was "isolated" in guinea pigs that further attempts to culture a "virus" were made
  • Many investigators tried to propagate Marburg "virus" in various cell cultures
  • In primary cells of Cercopithecus kidney, the species with which the agent was imported to Germany, Seigert et aI. (1968) found that the "virus" replicated without cytopathic effect (CPE)
  • On the contrary Haas et aI. (1968) observed gross CPE in primary Cercopithecus kidney cells
  • In primary Rhesus monkey kidney cells, the "virus" replicated but without CPE (Hofmann and Kunz, 1968)
  • Primary cells of human origin also propagated the "virus" yet May and Knothe (1968) could not observe CPE in human leucocytes but reported slight CPE in primary human amnion cells (May et aI., 1968)
  • Hofmann and Kunz could demonstrate replication of the "virus" in primary guinea pig embryo fibroblasts but no CPE was seen
  • In chick embryo cells, Hofmann and Kunz found a very slight "virus" replication while other investigators did not observe propagation at all (Smith et aI., 1967; May and Knothe, 1968)
  • Although Hofmann and Kunz found that permanent Cercopithecus kidney cells (strain GMK-AHl) produced high titers of "virus," they could not demonstrate any CPE
  • Kissling et aI. (1968) were more successful; they observed CPE in their cultures in the second day p.i., which was in total about the 4th-5th day
  • In the VERO cell line, the "virus" also propagated while no CPE was observed by Siegert et aI. (1968) and only slight CPE by Kissling et aI. (1968)
  • From cells of Rhesus monkey origin, heart cells (strain CMH) allowed only slight "virus" growth (Hofmann and Kunz, 1968), while in kidney cells (strain LLC-MK2) no "virus" replication was demonstrable (Smith et aI., 1967)
  • In the studies of Smith et aI. (1967) the Marburg "virus" propagated in L cells (mouse embryo cells) without CPE yet Hofmann and Kunz could not demonstrate any "virus" growth in those cells
  • Heart cells derived from guinea pigs also allowed "virus" replication without CPE (Kissling et aI., 1968)
  • The first reports of Marburg "virus-induced" CPE (interesting phrase here as CPE is only supposed to be "virus-induced") in cell cultures were by Zlotnik et aI. (1968) who found that the "virus" was adaptable to BHK21 cells
  • In the first passage typical inclusion bodies similar to those found in guinea pig liver, were seen in infected cells after 13 days and CPE appeared about the 23rd day
  • After a few passages, inclusion bodies as well as CPE appeared earlier (showing that the passaging caused the deterioration of the cells and the creation of the CPE, not the "virus")
  • In contrast to 3 other teams of investigators (Siegert et aI., 1968; Smitg et aI., 1967; May and Knothe, 1968), Hofmann and Kunz claimed that they could propagate Marburg "virus" quite well in HeLa strain however no CPE was observed
  • Other strains deriving from human sources were also tested for Marburg "virus" induced CPE as Kissling et aI. (1968) propagated the "virus" in foreskin fibroblasts
  • In the first passage of "virus" CPE was demonstrable but could not be reproduced in serial passages
  • In U cells, a stable cell line of human amnion, the agent also replicated but without CPE (Hofmann and Kunz, unpublished)
  • Hofmann and Kunz had previously tested many cell systems, but were unable to detect a cell line in which Marburg "virus" propagates with CPE until they came across the ELF (embryonal human lung fibroblasts) cell strain, in which CPE appears about the 3rd day and reaches its maximum about the 5th day after infection
  • However, they admitted that although changes were severe, they were never complete and eventually healthy cells may grow in and repair the lesions
  • Summarizing the sometimes conflicting results obtained by the various investigators, it was stated that cells deriving from mammals such as monkey, guinea pig, and hamster and human cells were susceptible to the "virus" as often high titers were produced by the cells, although as a rule no gross cytopathic changes could be observed
Fear Propaganda # 2

We are currently living in a time where novel "viruses" and old classics are seemingly breaking out in various parts of the world. Each of these outbreaks are presented by the media as potential epidemics/pandemics waiting to happen, if not now then definitely in the near future. We are being continually primed for this eventuality. What is interesting is that most of these diseases share the same non-specific symptoms including a flu-like illness and some form of rash. The diseases seem to be presenting in patients in atypical ways in non-endemic countries where the patients have no history of travel to known hotspots nor contact with any animals assumed to be carriers. As clinical diagnosis is impossible due to the overlapping symptoms, fraudulent  PCR tests are being used to generate cases.

The Marburg "virus" is the latest in this "viral" merry-go-round to make an appearance. Listening to the MSM, this "highly contagious virus" has the potential to explode into the world unless it is prevented immediately, even though there are no known treatments nor vaccine which are said to be successful against it. The recent "outbreak" in Ghana infected four people while the previous "outbreak" in Guinea in 2021 infected just one. To date, there have been a grand total of 475 cases of the Marburg "virus" worldwide since its "discovery" in 1967. Is this really the "highly contagious, virulent, and lethal virus" we have been sold?

Looking into the history of the "virus" paints an entirely different picture than the one sold by the MSM. Not only was the initial outbreak among polio vaccine researchers considered not alarming from the start, the patients were treated at home for up to 10 days. Those who were eventually admitted to the hospital were the ones who ultimately succumbed as quickly as one day after admission. One patient, who was considered severely ill, never sought hospital treatment and made a full recovery. Without knowing the exact treatments given to the patients prior to and immediately after admission to the hospital, one must wonder whether the treatments caused the severity of the symptoms seen in those who ultimately succumbed to the disease.

The discovery process for the novel "virus" creates an even more convincing case that there was never any new pathogen detected. First of all, no "virus" was ever purified nor isolated directly from the fluids of a sick human nor monkey. The only evidence used to claim the existence of the Marburg "virus" comes entirely from Guinea pig experiments where unpurifued goo and tissues were injected and serially passaged in the animals. After experimentally sickening the animals, non-specific antibody testing was performed in order to find Negri-like inclusions (said to be specific to rabies but shown repeatedly not to be) in the spleens and livers of the Guinea pigs, and then blood samples were sent for electron microscopy imaging in order to find the "virus." The hunt for the "virus" particles was long and the initial experienced researcher was unable to find anything after a day-and-a-half of searching. It wasn't until he left for lunch that his less-experienced lab assistant was able to find the "virus" after under an hour of looking. The filament-like particles were chosen as the representative for the Marburg "virus" due to their uniqueness and length. However, as admitted by lead researcher Rudolf Siegert, the particles were morphologically similar to many "viruses," including the rabies "virus" associated with the aforementioned Negri bodies. We can also find these filament-like forms associated with other "viruses" such as mumps, measles, parainfluenza, and many others.

According to Werner Slenczka, a man intimately involved in generating these EM images, the samples were contaminated by many microbial agents and even "paramyxoviruses" that made the interpretation difficult. He stated that the search for the "viral" particles was fatiguing and often frustrating. This confirms that the images used as evidence for the existence of the Marburg "virus" came from unpurified contaminated samples and thus there is no way to be able to state that the particles associated with the Marburg cases are in fact a "virus" at all. Slenczka also admitted that the monkeys assumed to be the source of the "virus" were never sick at any point and were used in other labs which never experienced any outbreaks whatsoever.

Even more interesting is that the attempts to "isolate" a "virus" were admitted to be failures. Early attempts to propagate the "virus" in cell cultures repeatedly ended in the lack of evidence of any "virus." However, this did not stop researchers from trying numerous cell lines for culturing until they got the results they wanted to see. After successive trial-and-error resulting in confusing, conflicting, and contradictory results, it was decided that, while the Marburg "virus" could propagate in cell cultures, it did so without producing the cytopathogenic effect (CPE), the very criteria used by virologists to indirectly "see" that the "virus" has highjacked the cell in order to replicate.

What we are left with regarding the Marburg "virus" are non-specific symptoms of disease associated with non-specific Negri-like inclusions in tissues and particles claimed to be unique "viral" structures that are in fact morphologically similar to many other "viral" particles. We also have a "virus" that is said to propagate in cell culture while not producing the very effect looked for to determine a "virus" is present within the sample. In other words, the Marburg "virus" is yet another in a long line of names given to the same symptoms of disease represented by the same random particles. It is just another fraudulent theatrical production put forward by the pseudoscience known as virology.

ViroLIEgy
24 Aug 2022 | 2:58 pm

Debating Virology With the Fakeologist


Last night marked my third time on the Fakeologist show and as usual, it was a fun and enlightening experience. We focused our attention on the recent "virus" debate drama with Steve Kirsch. For those unfamiliar with the situation, Steve is a serial entrepreneur and a Silicon Valley philanthropist who is trying to get those of us who were involved in the No "Virus" Challenge to pony up a million dollars to debate his "experts." I previously addressed this divide and distract tactic here. We also discussed those who are leading the anti-vaccination movement who still push the "virus" myth and are unwilling to look at and/or discuss the lack of scientific evidence supporting virology. The bottom line is that the time for debating the existence of "viruses" based on the current pseudoscientific evidence is over. It is time for the methods of virology to be put through the proper scientific validation process with proper controls. Only then can this 'debate begin to be settled once and for all.

FAK597-Mike Stone

Related posts brought up during our discussion:

Debunking the Nonsense:

https://viroliegy.com/2022/07/22/debunking-the-nonsense/

Science, Pseudoscience, and The Germ Theory of Disease – Dr. Jordan Grant

https://viroliegy.com/2022/06/21/science-pseudoscience-and-the-germ-theory-of-disease-dr-jordan-grant/

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