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Preface
This essay draws from Virus Mania: Corona/COVID-19, Measles, Swine Flu, Cervical Cancer and Other Viral Diseases—Why Vaccination, Profits, and Coercion Do Not Protect Us (3rd edition, 2021) by Torsten Engelbrecht, Claus Köhnlein, and Samantha Bailey. The book documents a fundamental problem in virology: the scientific standards established in the 1950s for virus identification were quietly abandoned in the 1960s when researchers couldn’t find the viruses they were looking for. What follows examines the evidence for this claim and its implications for modern virus detection methods.
The Standard Before It Fell: 1950s-1962
At the beginning of the 1950s, virologists established a consensus: purification was essential for virus identification. Under certain conditions, even healthy cells produce particles that look like tumor viruses. The only way to differentiate actual virus particles from virus-like particles was complete purification followed by electron microscopy.
The electron microscope, first patented in 1931, made viruses theoretically visible for the first time. Unlike bacteria and fungi, which appear under light microscopes, viruses measure only 20-450 nanometers across. Light microscopes can resolve down to approximately 0.2 micrometers; electron microscopes achieve resolution of approximately 0.1 nanometers. This thousand-fold improvement in resolution created the possibility of seeing viruses directly.
But seeing alone wasn’t enough. The particles had to exist in purified form. Without purification, researchers couldn’t distinguish between actual viruses and the cellular debris, exosomes, and other particles that cells naturally produce. This principle was confirmed at an international meeting of the Pasteur Institute in 1972 and “endured in the early 1980s,” according to Val Turner of the Perth Group, an Australian research team.
Turner described the logic in straightforward terms: “Think of it like a paternity suit in which DNA evidence will be used and the accused is HIV and the child is a human. The crux of the case is proof that the DNA you found in the human is the same DNA you found in the accused. For the latter, you have to have rock solid proof the DNA came from the accused. Given that in cell cultures all sorts of particles appear, only some of which are viruses, you have to prove that (a) a particular particle is a virus; and (b) your DNA comes from that particle. How can you prove (a) without using electron microscopy and without purification?”
In 1962, the Cold Spring Harbor Conference reinforced this standard. André Lwoff, who would receive the Nobel Prize for medicine three years later, designated electron microscopy as likely the most efficient method of proving viruses’ existence. He suggested investigating viruses with this procedure and dividing them into classes.
The principle hadn’t changed in centuries. As Turner noted: “Has Archimedes’ principle ‘moved on’ that says that a body immersed in a fluid is buoyed up by a force equal to the weight of the displaced fluid? Do solid objects no longer displace their own volume of liquids? If everything has to be ‘up to date’ then in ten years nothing that is up to date now will be up to date then.”
By 1960, electron microscopy was held to be the best way of identifying viruses in cell cultures. Laboratories worldwide directed their efforts toward observing particles in cancer cells with ever-improved methods of electron microscopy. Pathology professor Etienne de Harven, whose research career included 25 years at the Sloan-Kettering Institute in New York, watched this process unfold directly.
The standard was clear: purify the particles, image them with an electron microscope, biochemically characterize them. Only then could researchers claim to have identified a virus.
The Cancer Virus Hunt Collapses: 1959-1968
Cancer researchers had a fixed idea that viruses were definitely cancer triggers. They spent years trying to prove the presence of viruses in human cancer cells using electron microscopy. The efforts were unsuccessful.
In 1959, researcher Hagenaus reported in the journal Etude du Cancer about difficulties identifying any typical virus particles in a wide range of breast cancer samples. In 1964, scientists Bernhard and Leplus were unsuccessful, even with electron microscopy’s assistance, in finding virus particles presumed to play a role in the development of Hodgkin’s lymphoma, lymphoid leukemia, or metastases.
De Harven observed the pattern: “One only found virus-like particles from time to time—while viruses of a certain types could never convincingly be seen.”
The scientific community tends not to publicize negative results—”publication bias” in scientific language. Journals protect commercial interests rather than scientific integrity. Scott Kern of Johns Hopkins University, editor of the online Journal of Negative Observations in Genetic Oncology, explained one motive: “In some cases, withholding them keeps rivals doing studies that rest on an erroneous premise, thus clearing the field for the team that knows that, say, gene A doesn’t really cause disease B.”
But the cancer virus hunters’ failures were so universal that articles leaked into medical publications. The failures accumulated. Researchers couldn’t find cancer viruses in human cells no matter how hard they looked.
These scientific studies didn’t stop the virus hunters. Instead of questioning the cancer-producing virus model, they attacked the methodology. Thin-sections had proved effective countless times and worked perfectly with mice. But virus hunters needed a scapegoat. They claimed the production of thin-sections was too laborious and time-consuming. Pharmaceutical companies were offering fast cash for quick fixes.
Scientists turned to the dye method, which was simpler and faster. With the dye method, certain particles like DNA and RNA were marked in color and then electron micrographed. The results were scientifically disastrous. The air-drying process necessary for staining caused particles to become totally deformed. They appeared as particles with long tails—full-blown artificial products of the laboratory. They looked exactly like many other non-viral cellular components. Determining whether a virus or a non-viral particle had been found became impossible.
A few scientists acknowledged the dye method was dubious. But instead of returning to thin-sections, they began attacking electron microscopy technology itself. Other researchers were so anxiously preoccupied with finding cancer viruses that they overlooked the worthlessness of dye method results. They theorized that the “tailed” particles were a certain type of virus. Virus hunters were remunerated with research money for this work.
Cow’s milk and mother’s milk were tested for the presence of “tailed” particles in the rush to prove viruses could produce cancer. Molecular biologist Sol Spiegelman warned against breastfeeding in October 1971. His message made numerous lurid media headlines. These researchers brushed aside the fact that not a single retrovirus has been isolated from breast cancer tissue. Shortly thereafter, Spiegelman was quoted in Science saying, “one can’t kick off fear mongering on this scale if one doesn’t exactly know if a virus particle is the cause.”
By the time this became clear in the late 1960s, viral oncology had achieved a dogmatic, quasi-religious status. Etienne de Harven described what happened next: “If viral particles cannot be seen by electron microscopy in human cancers, the problem was with electron microscopy, not with the dogma of viral oncology.”
Viral particles similar to those readily recognized in cancerous and leukemic mice had never been seen in human cancers. The hypothesis that cancer might be caused by viruses was formulated in 1903. Even today it has never been convincingly demonstrated. But rather than abandon the hypothesis, researchers decided the methodology was at fault.
The Great Substitution: 1970s
Mainstream viral research drifted purposefully away from the established viral proof model. In 1970, Howard Temin and David Baltimore described activity of the enzyme reverse transcriptase in connection with cancer viruses. Their research seemed so significant that they were awarded the Nobel Prize in 1975.
Reverse transcriptase transforms RNA in RNA viruses into DNA, enabling virus multiplication. Researchers rushed to assume that reverse transcriptase was something very typical of retroviruses. The logic went: if we observe reverse transcriptase activities in our test tubes, then we can be sure that a retrovirus is present as well.
This conclusion had a problem. In 1972, Temin and Baltimore themselves had stated that “reverse transcriptase is a property that is innate to all cells and is not restricted to retroviruses.” Even Françoise Barré-Sinoussi and Jean Claude Chermann, who would later become important co-authors of Luc Montagnier’s 1983 HIV paper, concluded in 1973 that reverse transcriptase is not specific to retroviruses but rather exists in all cells.
If the enzyme reverse transcriptase is present in all cells, how can we conclude from its presence in a cell culture that a retrovirus is present? And even if the enzyme reverse transcriptase were specific for retroviruses, can the discovery of a process be considered evidence for the isolation of an object? If a particle hasn’t been purified and isolated, how do we know which proteins or enzymes belong to it?
The Perth Group later asked these questions directly to HIV researchers. They asked whether Luc Montagnier et al. had provided conclusive studies proving HIV isolation. They were sent the article “Molecular Cloning of LAV” by Montagnier et al., published in 1984 in Nature. In it, Montagnier et al. say “they have sought to characterize LAV by the molecular cloning of its genome.” The authors already assume that the genome from which they are making the clones originates from HIV. The argument is circular.
Nevertheless, the presence of reverse transcriptase was presumed sufficient to prove the existence of a retrovirus and even a viral infection of the tested cells. This dogma became fixed in the minds of mainstream researchers. It opened the floodgates to allow indirect virus detection methods—surrogate markers—to take the place of direct detection procedures.
Molecular biology was taking a totally dominant posture in viral research. “Molecular markers” for retroviruses were invented and substituted for the absent viral particles. This permitted the viral hypothesis to survive for another ten years, until the late 1970s, with increasingly generous support from funding agencies and pharmaceutical companies.
By 1980, the failure of this line of research was becoming embarrassingly evident. The closing of some viral oncology laboratories would have been inevitable. Then in 1981, five cases of severe immune deficiencies were described by a Los Angeles physician, all among homosexual men who were also all sniffing amyl nitrite, abusing other drugs, abusing antibiotics, and probably suffering from malnutrition and sexually transmitted diseases.
A logical hypothesis would have been that these severe cases of immune deficiency had multiple toxic origins. This would have amounted to incrimination of these patients’ lifestyle. Such discrimination was politically unacceptable. Another hypothesis was found: these patients were suffering from a contagious disease caused by a new retrovirus. Scientific data in support of this hypothesis was—and remains—totally missing.
Instantaneous and passionate interest from cancer virus researchers and institutions erupted. All the old virus hunters from the National Cancer Institute put new signs on their doors and became AIDS researchers. The methodology they brought with them was the same methodology that had failed to find cancer viruses: indirect detection through molecular markers, no purification, no electron microscopy of purified particles.
Modern Virus Detection Without Viruses
In 1983, in a paper printed in Science, researcher Luc Montagnier of the Institute Pasteur in Paris asserted that his research team had found a new retrovirus, later named HIV. This was claimed only after reverse transcriptase activity had been observed in the cell culture. There was no scientific proof for this conclusion.
Even Montagnier admitted in an interview with the journal Continuum in 1997 that even after “Roman effort,” with electron micrographs of the cell culture with which HIV was said to have been detected, no particles were visible with “morphology typical of retroviruses.” If even retrovirus-like particles cannot be recognized in these electron micrographs, HIV—allegedly a very specific retrovirus—cannot be detected.
All electron micrographs of so-called HIV taken from the mid-80s on come not from a patient’s blood but from “souped-up” cell cultures. In some cases the cells have been cooked up for a week in a lab Petri dish. Hans Gelderblom of the Robert Koch-Institute in Berlin attempted to make scientific sense of co-culturing techniques in 1997, but his article left out purification and characterization of the virus. Merely the protein p24 was found, which does not prove the particles are HIV. Mainstream AIDS researchers claim proteins like p24 and p18 are specific to HIV and use them as HIV markers, but they are found in numerous so-called “uninfected” human tissue samples.
The same pattern appears with SARS-CoV-2. Researchers contacted by Torsten Engelbrecht and Konstantin Demeter conceded they did not complete purification. The authors of five relevant papers cited in connection with the detection of SARS-CoV-2 all admitted their electron microscope images do not show completely purified viruses. When asked if purification was unnecessary, no one wrote back suggesting that complete purification is not a necessary step for solid virus detection.
Charles Calisher, a seasoned virologist, was asked whether he knows of a single paper in which SARS-CoV-2 had been isolated and then truly purified. His answer: “I know of no such a publication. I have kept an eye out for one.”
Canadian biostatistician Christine Massey and Michael Speth from New Zealand submitted Freedom of Information applications to institutions around the world to obtain documents describing the complete purification of SARS-CoV-2 from an unaltered sample of a sick patient. As of January 2020, all 46 responding institutions utterly failed to provide or cite any such documents. Germany’s Ministry of Health ignored their request altogether.
Michael Laue from the Robert Koch-Institute wrote in an email: “I am not aware of a paper which purified isolated SARS-CoV-2.” The U.S. CDC wrote in a document updated on July 13, 2020: “Since no quantified virus isolates of the 2019-nCoV are currently available.”
If no particle purification has been done, how can one claim that the RNA obtained is part of a viral genome? The RNA sequences that scientists extracted from tissue samples and which the SARS-CoV-2 RT-PCR tests were “calibrated” to are based on faith alone, not on sound research.
Researchers took samples from the throat or lungs of patients, ultracentrifuged them to separate the larger from the smaller molecules, and then took the supernatant—the upper part of the centrifuged material. This is what they called their “isolate.” But this supernatant contains billions of different micro- and nanoparticles, including extracellular vesicles and exosomes, which are produced by our own bodies and are often indistinguishable from viruses. A study published in May 2020 in the journal Viruses stated: “Nowadays, it is an almost impossible mission to separate EVs and viruses by means of canonical vesicle isolation methods, such as differential ultracentrifugation, because they are frequently co-pelleted due to their similar dimension.”
How do you extract a specific virus from this huge mixture of billions of indistinguishable particles? You cannot, unless you have purified the particles beforehand and defined their genetic structure and disease-causing properties.
The scientists “create” the virus by PCR. They take artificial and hypothetical primers—previously existing genetic sequences available in genetic banks—and put them in contact with the supernatant containing tens of billions of RNA and DNA molecules. If the primers attach to something in that mixture, they conclude that whatever attached to the primers is the new virus.
The primers used are an infinitesimal fragment of the alleged genome of the virus—only 18 to 24 bases each. The SARS-CoV-2 virus is assumed to consist of 30,000 bases. The primers represent only 0.07 percent of the virus genome.
Antibody tests are equally problematic. They prove the existence of antibodies, not the virus or particle itself to which the antibody tests react. As long as the virus or cell particle has not been precisely defined, no one can say what these antibody tests are reacting to. They are “nonspecific” in medical terminology.
PCR tracks down genetic sequences—little genetic snippets—and replicates them a million-fold. As with antibody tests, PCR probably has significance because it detects some sort of immune reaction or cellular activity. But a virus with indeterminate characteristics cannot be proven by PCR any more than it can be determined by an antibody test. The exact virus determination has not been carried out. Even Robert Gallo conceded this in court in 2007.
In 2001, fourteen renowned virologists of the “old guard” directed an appeal to the young high-technology-focused generation of researchers, published in Science: “Modern methods like PCR, with which small genetic sequences are multiplied and detected, are marvelous [but they] tell little or nothing about how a virus multiplies, which animals carry it, how it makes people sick. It is like trying to say whether somebody has bad breath by looking at his fingerprint.”
An early 2006 article in the Deutsches Ärzteblatt about researchers who thought they had discovered new “exotic” bacteria with PCR noted: “only genetic traces of the pathogen are detected [with the PCR]. From this, it cannot automatically be concluded that complete bacteria exist as well.”
The PCR tests used to identify COVID-19 patients do not have a valid gold standard to compare them with. Tests need to be evaluated by comparison with the most accurate method available. For a pregnancy test, the gold standard is the pregnancy itself. Australian infectious diseases specialist Sanjaya Senanayake stated: “If we had a new test for picking up [the bacterium] golden staph in blood, we’ve already got blood cultures, that’s our gold standard we’ve been using for decades, and we could match this new test against that. But for COVID-19 we don’t have a gold standard test.”
The product descriptions of the RT-qPCR tests for SARS-CoV-2 state they are “qualitative” tests, contrary to the fact that the “q” in “qPCR” stands for “quantitative.” If these tests are not quantitative, they cannot show how many viral particles are in the body. To talk about actual illness, a patient would need millions and millions of viral particles actively replicating in their body.
The CDC, WHO, FDA, and RKI assert the tests can measure “viral load”—how many viral particles are in the body. But this has never been proven. Even the term “viral load” is deceptive. If you asked what viral load means at a dinner party, people would assume it means viruses circulating in the bloodstream. In reality, it refers to RNA molecules.
To prove the PCR can measure how much a person is burdened with a disease-causing virus, a specific experiment would be required. Take tissue samples from a few hundred people. Have testers who know nothing about the test subjects perform PCR tests on the samples. Identify patients with high loads of the target genetic material. Then un-blind those patients. They should all be sick, because they have so much virus replicating in their bodies. Are they really sick—or are they healthy?
This experiment has not been done.
The Consequences
In 2005, Torsten Engelbrecht contacted the Robert Koch-Institute and requested studies that indisputably show that SARS, hepatitis C, Ebola, smallpox, and polio viruses and the BSE causative agent have been proven to exist—complete purification, isolation, definition of biochemical properties, plus electron micrographs. He requested studies that indisputably show these viruses cause disease. He requested at least two studies that indisputably show vaccinations are effective. Despite repeated questioning, not a single study was named.
The same request was made to the German Friedrich-Loeffler-Institut regarding H5N1. No studies delivering clear-cut proofs were received from either the RKI or the FLI.
Mainstream virus-science left the road of direct observation of nature and decided to go with indirect “proof” through procedures like antibody and PCR tests. These methods lead to results that have little to no meaning. The 1950s consensus was abandoned not because new evidence disproved it, but because researchers couldn’t find what they were looking for.
The hypothesis that cancer might be caused by viruses was formulated in 1903, more than a century ago. It has never been convincingly demonstrated. Viral particles similar to those readily recognized in cancerous and leukemic mice have never been seen in human cancers. When this became clear in the late 1960s, the problem was declared to be with electron microscopy, not with the dogma of viral oncology.
Viruses that purportedly threaten to wipe out humanity—H5N1, SARS virus, SARS-CoV-2—have evidently never been seen by anyone in properly purified form. The procedure rarely gets carried out in modern viral research. Around 1960, before contemporary molecular biology arose, electron microscopy was held to be the best way of identifying viruses in cell cultures. Now it has been replaced by indirect methods that cannot prove what they claim to prove.
The PCR tests are explicitly labeled “Research Use Only (RUO), not for diagnostic purposes” in their user manuals, according to evidence brought to court in the Netherlands. The CDC and FDA admit the SARS-CoV-2 RT-PCR tests are not suitable for diagnosis of SARS-CoV-2 infection. The instructions for use of the PCR tests explicitly state they are not intended for what they are overwhelmingly used for: diagnosis.
Antibody tests, PCR viral load tests, and helper cell counts are surrogate markers—alternative methods by which doctors determine whether someone is infected with a virus. Instead of investigating whether real disease symptoms have occurred, doctors look at laboratory data. Often enough, surrogate markers have led to misdiagnosis.
Heinz Ludwig Sänger, professor of molecular biology and 1978 winner of the Robert Koch Prize, stated that “HIV has never been isolated, for which reason its nucleic acids cannot be used in PCR virus load tests as the standard for giving evidence of HIV.”
Kary Mullis, who received the 1993 Nobel Prize in Chemistry for the invention of PCR, stated: “The PCR test doesn’t tell you that you are sick. These tests cannot detect free, infectious viruses at all.”
The standard was established in the 1950s: purify the particles, image them with an electron microscope, biochemically characterize them. When researchers in the 1960s couldn’t find cancer viruses in human cells using this standard, they blamed the methodology rather than their hypothesis. They invented molecular markers to substitute for the absent viral particles. Modern virology inherited this substitution and built an entire edifice of virus detection on methods that cannot prove a virus exists without first isolating that virus.
No virus has ever been properly isolated according to the standards virologists themselves established in the 1950s. The electron microscope problem is not a problem with electron microscopes. It is a problem with what happens when evidence doesn’t support a hypothesis and researchers decide to change the evidence rather than the hypothesis.
References
Engelbrecht, Torsten, Claus Köhnlein, and Samantha Bailey. Virus Mania: Corona/COVID-19, Measles, Swine Flu, Cervical Cancer and Other Viral Diseases—Why Vaccination, Profits, and Coercion Do Not Protect Us. 3rd edition. Books on Demand, 2021.
Engelbrecht, Torsten, and Konstantin Demeter. “COVID-19 PCR Tests Are Scientifically Meaningless.” OffGuardian, June 27, 2020.
de Harven, Etienne. “The Recollections of an Electron Microscopist.” Reappraising AIDS, November/December 1998.
de Harven, Etienne. “Of Mice And Men: Viral Etiology Of Human Cancer: A Historical Perspective.” Continuum, Summer/Fall 2001.
Enserink, Martin. “Virology: Old Guard Urges Virologists to Go Back to Basics.” Science, July 6, 2001.
Montagnier, Luc, Françoise Barré-Sinoussi, and Jean Claude Cherman. “Isolation of a T-Lymphotropic Retrovirus from a Patient at Risk for Acquired Immune Deficiency Syndrome (AIDS).” Science, May 20, 1983.
Temin, Howard, and David Baltimore. “RNA-Directed DNA Synthesis and RNA Tumor Viruses.” Advances in Virus Research 17 (1972): 129-186.
Centers for Disease Control and Prevention. “CDC 2019-Novel Coronavirus (2019-nCoV) Real-Time RT-PCR Diagnostic Panel: For Emergency Use Only, Instructions for Use.” Updated July 13, 2020.
“The Role of Extracellular Vesicles as Allies of HIV, HCV and SARS Viruses.” Viruses, May 2020.