The “Virus” Deception: Case Studies in Pseudoscience — Part 1: The “Lipovirus”

This is a lengthy article from Mike Stone’s substack and so i am only including the first part of it.  You can see the full article at the link at the bottom….

How a speculative agent with no direct evidence was framed as a causative “virus.”

In the 1950s, virology began to emerge as a distinct discipline, separating itself from bacteriology. For the first time, it was (falsely) recognized as a legitimate scientific field. This shift was largely due to the introduction of the cell culture technique by John Franklin Enders in 1954. This method, still used by virologists today, asserts “viral” presence based on lab-created, artificial effects observed in cultures of human and animal cells.

Around the same time, electron microscopy became more widely available, allowing researchers to peer into unpurified culture soup and label random particles from the destruction of these cells as “viruses.” After decades of vagueness, in 1957, French microbiologist André Lwoff offered a consensus definition for the invisible entities virologists claimed to be studying. Journals were launched to publish the work of these newly anointed experts. It was a decade of enormous “progress” for the pseudoscientific field.

Emboldened by these tools and techniques, “virus” hunters began “discovering” new “viruses” with remarkable ease—despite never having the actual agents in hand to study. But in their rush to interpret indirect, nonspecific, and artificial lab effects as proof of “viral” entities, virologists set the field on a path of misinterpretation, speculation, and pseudoscience.

This pattern soon played out across a range of illnesses in need of a theoretical “pathogen.” One prominent example was hepatitis. According to the editorial Candidate Viruses in Hepatitis, researchers had previously relied on serologic “antibody” testing and human volunteer inoculation in an attempt to prove a “viral” cause for the disease, but the invisible culprit remained elusive. Results that appeared promising for one group were often not reproducible by others—a direct violation of a foundational principle of the scientific method. Yet despite lacking a purified “virus” and failing to replicate findings, researchers still labeled these mysterious agents as “candidate viruses,” signaling nothing more than an unproven suspicion of causation.

“Identification as an agent likely related to hepatitis in turn has relied mainly on serologic (neutralization) tests and inoculation of human volunteers followed by reproduction of clinical features of the disease. A problem precluding maximum accomplishment has been the inability of different research laboratories to reproduce the same results. In addition, essential as repeated isolations from the original material by any given laboratory might seem, this has not always been the case.”

The first “candidate virus” for hepatitis was “discovered” by Werber Henle in 1954 using Maitland-type chick embryo tissue cultures. However, his attempts to demonstrate an “infectious virus” failed: the inoculated volunteers showed no serologic response, and no “immunity” could be observed upon re-challenge.

“The first culture-derived observations on infectious hepatitis were reported by Henle, working with Maitland-type chick embryo tissue cultures. Serological findings in volunteer subjects inoculated with the fluid remained negative, and no immunity could be demonstrated in subsequent challenge with the original agent.”

Over the next decade, numerous labs claimed to isolate “candidate viruses” from hepatitis patients using a variety of human and animal tissue cultures. These included:

• Rightsel and Boggs: Claimed hepatitis-like illness was caused by injection of “infected” culture fluid.
• Davis: “Isolated” the so-called San Carlos agents (“adenoviruses”) from children’s stool, but no direct link to hepatitis was found.
• Chang: Reported a “lipovirus” from hepatitis patients’ blood, but could not classify it or establish any association.
• O’Malley: “Isolated” the “A-1 virus” from serum; results were inconsistent, and serologic relationships were unclear.
• Bolin et al.: Claimed “isolation” of a “virus” from volunteers given a known serum hepatitis sample.
• Hillis: Observed cell damage from hepatitis patient serum, but the effect was lost in serial passage.
• Hsiung et al.: Found a “myxovirus” (DA “virus”) in a fatal case, but refrained from claiming causation.
• Schneider et al.: Detected agents in both chronic and acute cases using canine lung tissue.
• McKees: Claimed to “isolate viruses” on monkey kidney tissue from hepatitis patients, reportedly transmissible to suckling mice.

Despite these numerous claims, no consistent or definitive evidence ever established a direct causal link between any of these agents and hepatitis. Researchers experimented with various tissue and cell cultures, hoping to find a formula that would recreate the disease and produce the expected indirect signs of “infection.” When a particular result appeared to match their expectations, they rushed to assume a “viral” cause. They would name a supposed “virus” and then treat it as if it had been proven to cause the artificial, lab-created effects they had generated. In doing so, they engaged in fallacious reasoning—such as affirming the consequent and post hoc fallacies—deceiving themselves into believing that the invisible culprit was in hand.

Fortunately, some researchers were honest enough to acknowledge when the evidence failed to support early assumptions of a “viral” cause. In many cases, the indirect findings not only fell short of being sufficient—they ultimately pointed away from the “viral” hypothesis altogether. One notable example comes from the work of Dr. Robert Shihman Chang, a pioneer in cell culture. He was among the first to establish immortalized lymphoid cell lines using the “Epstein-Barr Virus,” focusing primarily on developing cell lines that could support “viral” growth for in vitro study. During his investigations into hepatitis, which led to the emergence of the so-called “lipovirus” in 1960, he inadvertently demonstrated how reliance on indirect evidence—such as CPE, “antibody” tests, and electron microscopy—paired with fallacious reasoning can lead researchers to mistakenly believe they’ve discovered a new “virus,” only to later realize the trail of pseudoscientific breadcrumbs led nowhere. This is the story of how a virologist was both misled by assumptions and deceived by the very methods believed to prove a “viral” cause.

This article delves into some technical details. To fully grasp its significance—especially for those unfamiliar with the fallacious and pseudoscientific methods commonly used in virology—it’s helpful to review a few foundational articles first. These provide essential background and context to better understand the depth of the deception involved.

I recommend starting with the following:

• Intro to ViroLIEgy
• ViroLIEgy 101: Logical Fallacies
• The Chain of Causation
• The Mirror Cytopathic Effect
• “Virus-like” Particles

Reading these will offer a clearer lens through which to view the flawed reasoning and assumptions that underpin the virological narrative exposed in this article.

Go here for the full article: https://mikestone.substack.com/p/the-virus-deception-case-studies

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