The “Virus” Deception: Case Studies in Pseudoscience — Part 2: SMON Says

"Act like a virus!"

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.