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

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

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/

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

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.

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. Porton 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 Porton 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 Southern 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.

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

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 guinea pigs (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?