The “Virus” Deception: Case Studies in Pseudoscience — Part 2
In the first part of this series, I examined how fallacious reasoning and indirect methods commonly used by virologists can deceive them into believing they’ve found a “virus” when no such thing has been demonstrated
I focused on the case of Dr. Robert Shihman Chang and the so-called “lipovirus,” a phenomenon that arose in 1954 when artificial cytopathic effects (CPE) were observed during early cell culture experiments.
These effects were interpreted as evidence of a “transmissible cytopathic agent.” Instead of first purifying and isolating any presumed “viral” particles, researchers attempted to retroactively fit the observed effects to the “viral” hypothesis.
Despite the absence of purified, isolated, photographed, and characterized “viral” particles, Dr. Chang and others pursued serological tests in an attempt to establish a “viral” identity—claiming that this presumed “virus” existed both in those sick with hepatitis and in the general population via the detection of “antibodies.”
However, any contradictory evidence—particularly findings that did not conform to the predetermined expectations of what a “virus” should be—was ignored or dismissed.
Eventually, independent research revealed that the observed CPE was not caused by a “virus” at all, but by an ameboid. What had been considered evidence of a “viral” cause turned out to be a case of mistaken identity.
Dr. Chang ultimately accepted this reinterpretation, and the “viral” hypothesis collapsed.
This case stands as a damning example of how a researcher can deceive himself through circular reasoning and indirect, assumption-laden evidence—constructing an imaginary cause on a foundation lacking scientific rigor.
Yet, this was not an isolated incident.
Around the same time the “lipovirus” was being investigated, Japan faced a severe neurological outbreak. This debilitating condition was marked by the degeneration of the spinal cord, optic nerve, and peripheral nerves, and led to widespread panic and misattribution of cause—much like in the “lipovirus” case.
The clinical features included:
- Progressive weakness and numbness in the legs, sometimes leading to paralysis
- Visual impairment or blindness due to optic neuritis
- Loss of reflexes and sensation in affected areas
- Urinary and fecal incontinence
- Cognitive changes and alterations in personality
Symptoms typically developed over weeks to months, sometimes leading to severe disability or even death if left untreated. In the early stages, the condition was mistaken for benign encephalomyelitis, multiple sclerosis, polio, or Devic’s disease.
In fact, it was once called “Non-specific encephalomyelitis with abdominal symptoms” due to the lack of unique or distinguishing symptoms. The question was even posed as to whether or not the disease “constitutes a distinctive clinicopathological entity, since it is well documented that a variety of neurological disorders may be accompanied by acute abdominal conditions.”
However, as clinical and post-mortem evidence accumulated, it was decided that this was a distinct disease, marked by “unique,” non-inflammatory degenerative damage to the nervous system.
In 1965, the term Subacute Myelo-Optico-Neuropathy (SMON) was proposed to capture these features and its unknown cause, quickly gaining acceptance for its clarity and utility.
Several hypotheses were proposed to explain this seemingly new disease, including:
- Intoxication from agricultural pesticides, industrial waste, or heavy metals
- Excessive or improper drug use
- A metabolic disorder or vitamin deficiency
- A neuro-allergic condition, suggested by the sex and age distribution
- An “infectious” etiology
Unsurprisingly, the “infectious” hypothesis gained the most traction—an outcome this article will focus on. It was widely considered the most plausible explanation at the time.
As part of the investigation, multiple researchers claimed to have found “cytopathic agents” in the spinal cord, cerebrospinal fluid, blood, and feces of SMON patients. This gave rise to a wave of confidence that a new “virus” would be uncovered.
In the early 1970s, virologist Shigeyuki Inoue emerged as the leading proponent of the “viral” hypothesis for SMON, relying on the usual indirect and ultimately unconvincing pseudoscientific lines of evidence.
His claims gained traction not because they were conclusive, but because they aligned with prevailing assumptions in a field dominated by “virus-centric” thinking. At the time, Japan was still heavily invested in polio research, and many of the same virologists simply redirected their focus toward SMON.
Inoue’s findings—examined in detail below—were seen as legitimizing to the search for a “viral” cause. Yet in the end, the very data meant to support the theory helped dismantle it.
As this article will show, SMON is not merely an embarrassing footnote in medical history—it is a revealing case study in how institutional bias, scientific inertia, and the allure of the invisible “virus” can not only derail reason and prolong suffering, but also enable a culture of deception to masquerade as medical certainty.
The SMON episode began in Japan around 1955, when patients started reporting numbness or loss of sensation in the feet following bouts of gastrointestinal illness. These early symptoms were accompanied by impaired vision and difficulty walking due to progressive paralysis in the lower limbs.
By 1957, large outbreaks of the polio-like condition were reported across Japan, leading many to suspect a “contagious” cause. However, the disease’s nonspecific presentation created diagnostic confusion, particularly during Japan’s polio outbreak between 1960 and 1961.
Although SMON was eventually considered unrelated to polio, it was sometimes referred to as “adult polio” due to the similarity in symptoms and the overlap in timing with polio epidemics of the 1960s.
According to the paper Subacute myelo-optic neuropathy and cioquinol: An epidemiological case-history for diagnosis, abdominal symptoms nearly always preceded the neurological ones.
However, deaths from the disease were difficult to track, as SMON was frequently associated with other conditions. It was estimated that no more than 5% of patients actually died from SMON itself.
The primary neurological differential diagnosis was subacute combined degeneration (SCD) of the spinal cord. SMON also shared overlapping features with multiple sclerosis, pernicious anemia, various intestinal disorders (such as blind loops, strictures, and anastomoses), Coeliac disease, and toxic exposures to lead, mercury, arsenic, and thallium.
In its “less complete forms”—typically marked by abdominal symptoms and dysesthesia—SMON was difficult to distinguish from other causes of peripheral neuropathy and myelopathy. Since these “incomplete forms” accounted for the majority of cases, misdiagnoses were common and posed serious challenges to epidemiological investigation.
For nearly the entire course of the epidemic—from 1955 to 1970—SMON was widely believed to be an “infectious” disease. This belief was primarily supported by a consistent summer peak in incidence, reports of clustering among individuals who drank fecally contaminated water from the same sources, and claims by various researchers that they had isolated microbiological “pathogens” from affected patients.
An epidemiological case-history for diagnosis
THE DISEASE, AND A SUSPECTED CAUSE
During the mid- and late 1950s, doctors in Japan were consulted by increasing numbers of patients with an unusual combination of alimentary and neurological complaints.
The common clinical picture was of abdominal pain and/or diarrhoea, followed within a few days or weeks by painful dysaesthesiae; in addition to the predominantly sensory disturbances, upper and/or lower motor neurone signs occurred in just over 50 percent of cases, and visual disorders due to optic neuritis in about 28 percent (Sobue et al., 1971).
The disease was called subacute myelo-optic neuropathy, or SMON. Table I summarizes Kono’s (1971) list of SMON’s ‘cardinal’ and other symptoms; of particular importance is that the abdominal symptoms nearly always preceded the neurological.
Case-fatality from SMON itself is hard to assess because the disease was very often associated with other conditions, many having a poor prognosis; but it is likely that not more than five percent of SMON patients actually died of the disease itself.
On the other hand, probably 90 percent of patients were left with dysaesthesiae, and 50 percent with limb weakness, visual impairment, or both; 10 to 15 percent were completely disabled (Kono, 1971).
By the time the epidemic was over, some 10 000 Japanese were said to have developed SMON, a figure of the same order as the world wide total of thalidomide-deformed children.
The main epidemiological features of the disease are summarized in Table II; these have not been seriously contested by the protagonists or antagonists of the hypothesis on aetiology with which this review is concerned.
Subacute combined degeneration (SCD) of the cord is the main neurological differential diagnosis of SMON; multiple sclerosis has also to be considered.
In addition to pernicious anaemia, SCD may, of course, be associated with a number of intestinal disorders resulting in impaired vitamin B12 adsorption-such as blind loops, strictures, and anastomoses.
Coeliac disease, lead, mercury, arsenic, and thallium intoxications also give rise to both abdominal and neurological manifestations, so that SMON was by no means unique in these respects.
Neurologists are in general agreement that SMON exhibiting all its neurological features, visual, motor, and sensory, was a distinct and real clinical syndrome, but it is clear that in its less complete forms it was not easily distinguishable from other causes of peripheral neuropathy and myelopathy.
Since these incomplete forms (for example, abdominal symptoms and dysaesthesiae) accounted for most cases, opportunities for misdiagnosis were frequent, a fact with obvious implications for epidemiological studies.
For virtually the whole course of the epidemic, which ran from 1955 to 1970, SMON was regarded as probably being an infectious disease (Ogata and Jitsunari, 1970).
The main points in favour of an infective aetiology were a regular summer peak in incidence, and claims that the disease clustered in individuals drinking faecally contaminated water from the same source.
Various workers (see Kono, 1971) claimed to have identified or isolated microbiological pathogens. The newness of the disease, its predilection for the elderly rather than the young, and the absence of expected clinical and pathological features of infective disease (for example, in the cerebrospinal fluid) were reasons against the infective theory.
In his book Inventing the AIDS Virus, virologist Peter Duesberg recounted how the SMON epidemic in postwar Japan became a cautionary tale of scientific misdirection.
He highlighted how the research establishment, dominated by virologists, approached the disease with a rigid assumption: SMON had to be “infectious.”This untested premise shaped the entire investigation, leading “virus” hunters to fixate on identifying the “right virus” while largely ignoring or downplaying evidence that challenged the idea of “contagion.”
Assuming that the disease was “infectious,” researchers jumped to conclusions to confirm their assumptions. Clusters of cases in families and hospitals were taken as confirmation of “transmissibility,” despite the lack of clear transmission pathways or consistent patterns.
The seasonal spike in cases during late summer even prompted speculation about insect vectors. Meanwhile, early “non-infectious” hypotheses—such as exposure to environmental toxins or occupational hazards—were pushed aside, not because they were falsified, but because they didn’t fit the dominant paradigm.
As Duesberg observed, this kind of misplaced attribution—blaming microbes for conditions that may not be “contagious” at all—was not new. What made SMON notable was how long the “viral” theory persisted, despite mounting evidence to the contrary.
For over a decade, the assumption of a “viral” cause went unchallenged as the framework discouraged exploration of other possibilities, despite a lack of compelling evidence.
Duesberg recounted how, in May 1964—after years of uncertainty surrounding the polio-like disease—SMON became a formal topic of discussion at the 61st General Meeting of the Japanese Society of Internal Medicine.
During this meeting, researchers officially named the condition Subacute Myelo-Optico-Neuropathy (SMON) and agreed upon standardized diagnostic criteria. A formal research commission was soon launched by the Japanese Ministry of Health and Welfare, led by Kyoto University professor Magojiro Maekawa.
Among the virologists appointed to the commission was Reisaku Kono, a prominent figure in Japan’s virology community, effectively cementing a presupposed “viral” etiology as the guiding assumption.
The very structure of the investigation had been front-loaded with that assumption: they were not asking whether the disease was “viral”—they were tasked with identifying which “virus” was responsible.
The first major “breakthrough” came from Masahisa Shingu, a virologist at Kurume University and fellow commission member, who claimed in 1965 to have found an “echovirus”—a type of “enteric virus” first discovered during polio research—in the excretions of SMON patients.
Based on this, Shingu asserted he had found evidence of “infection” and concluded that this “orphan virus” had finally been matched with a disease. He enthusiastically published his findings, boasting that he had “isolated” the cause of SMON.
But the logic was flawed from the start. When subsequent researchers, including Kono himself, failed to replicate these findings or demonstrate “infection” in patients, the “virus” hypothesis should have been abandoned.
Instead, it lingered—not because of evidence, but because virology had become too institutionally committed to its own presumptions. Another wave of excitement followed in 1968, when two researchers reported the presence of a “Coxsackie virus”—another class of “enteric virus,” also discovered incidentally during polio research—in SMON patient tissue.
This too was later debunked, as the “discovery” turned out to be the result of accidental laboratory contamination.
This is taken from a long document. Read the rest here substack.com
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