The Mirror Cytopathic Effect

Written by Mike Stone on May 26, 2025. Posted in Current News

Science is the systematic study of the natural world. As outlined in Chapter 2 of Environmental Science, its fundamental goal is “to understand natural phenomena and to explain how they may be changing over time.”

To achieve this, science depends on empirical observation, logical reasoning, and controlled experimentation—most often guided by inductive reasoning.

The systematic process utilized to acquire scientific knowledge is known as the scientific method, and it begins with the observation of natural phenomena: events or processes that occur without human intervention and can be detected by the senses.

From these observations, scientists form hypotheses—falsifiable and testable explanations that define a presumed cause (independent variable) and predict an effect (dependent variable).

The National Academy of Sciences defines science as “the use of evidence to construct testable explanations and predictions of natural phenomena,” emphasizing that all scientific inquiry must be grounded in the observable world.

Any explanation that arises from phenomena not observed in nature—such as effects manufactured in laboratory conditions—cannot be tested, verified, or falsified, and therefore falls outside the bounds of science.

This distinction is critical when evaluating virology methods. The natural phenomenon under investigation—disease in a living host—is not being studied through direct observation or controlled replication of that condition. Instead, virologists rely on artificial methods that bear no resemblance to the phenomenon itself.

Rather than purifying and isolating presumed “viral” particles directly from the fluids of a sick individual and testing their “pathogenicity” through natural exposure to a healthy host—as would befit the study of disease and the proposed route of transmission—virologists conduct complex cell culture experiments.

In these procedures, an unpurified patient sample is added to a culture of cells—typically derived from animal kidneys or human cancer lines—and maintained for days in the presence of fetal bovine serum, antibiotics, antifungals, and other foreign substances.

If visible cellular damage or death occurs, this effect—called the cytopathic or cytopathogenic effect (CPE)—is interpreted as indirect evidence of a “virus.”

However, the cytopathogenic effect is not a naturally occurring phenomenon, but rather an artifact of the laboratory setup. It arises from removing cells from their natural environment and exposing them to artificial and often stressful conditions, including toxic chemicals, foreign sera, and other unnatural additives.

These factors alone are sufficient to cause cellular deterioration or death, regardless of any presumed “viral” presence.

This was acknowledged by John Franklin Enders, the man who brought this method to prominence in the mid-1950s. In a revealing 1954 paper titled Cytopathology of Virus Infections: Particular Reference to Tissue Culture Studies—published the same year as his influential measles study that showed CPE in the “uninfected” cultures—John Enders admitted that CPE could be triggered by many agents aside from “viruses.”

He acknowledged that cytopathic effects are influenced by numerous factors, both known and unknown. These include the age and type of donor tissue, the culture conditions, and environmental variables.

In other words, the cellular changes virologists attribute to a “virus” may have no connection to one at all.

“The phenomena mentioned above under Group 1 changes may be evoked by many noxious agents. Accordingly, they cannot alone be considered as necessarily the result of viral activity. To prove this certain control procedures (serial cultivation, prevention of changes by homologous antibody, etc.) must be applied. Familiarity, however, with the effects of a specific virus in a given cell system often enables the observer to conclude tentatively that this virus is responsible.”

“Of morphological indices of viral injury, the formation of inclusion bodies (Group 2 above) is the most characteristic, although again this process cannot be accepted as conclusive evidence of viral activity since certain chemical as well as other unknown factors may condition its development. Inclusion bodies were the first cytopathic changes to be sought for in vitro and employed as criteria of infection. As indices of viral multiplication, however, they are less useful than the changes of Group 1, because these structures can be unmistakably demonstrated only in stained preparations.”

“Cytopathogenicity in vitro is influenced by factors some of which are known while many remain to be defined. At the outset a few of those now recognized will be mentioned as an introduction to the review of recorded observations on the behavior of individual agents. Of primary importance is the species from which the cells are derived.

Analogous to the host range of a virus is its cytopathogenic range in cultivated cells. But correlation between susceptibility of the organism and its cells in vivo does not always exist. For although this correlation frequently obtains, the tissues of a susceptible species occasionally fail to support viral multiplication while the converse of this situation also occurs.

The age of the donor of tissue may influence cytopathogenicity. Just as young animals are frequently more susceptible to infection so their tissues may be more vulnerable to injury by the virus, yet again this correlation is not invariable. Most of the pertinent data indicate that acquired immunity to viral infections is not reflected by an increased cellular resistance, a fact advantageous from the technical point of view since it eliminates concern over the immunologic status of the donor animal.

The intensity and degree of cytopathic injury may vary according to the strain of virus or the conditions under which it has been propagated prior to its study in tissue culture. The investigator should be prepared to encounter such variations in the study of a number of representatives of a viral species. Moderate or weak cytopathogenicity may sometimes be enhanced by serial passage in vitro.”

In fact, a variety of “non-viral” factors have been shown to induce the same CPE in cell cultures. These include bacterial contamination, parasites, amoebas, chemical additives, antibiotics, antifungals, nutrient deprivation, environmental stress, and even the age-related breakdown of the cells themselves.

I have explored these factors in more detail in previous articles [here, here, and here].

Other notable factors that have been blamed for causing CPE in cell cultures include fibrinolytic agents, drugs, placental proteins, “virus-free” fecal samples that produced “profound” CPE resembling that attributed to “enteroviruses,” “immune” cells and “antibodies,” and the spontaneous degeneration of “virus-free” 12-week-old human embryonic tissue that mimicked the effects associated with the “cytomegalovirus.”

Even serum starvation—a routine step in virology protocols—has been repeatedly shown to induce cell death and morphological changes indistinguishable from the so-called CPE used to infer “viral” presence.

This has been demonstrated in published studies and confirmed by Dr. Stefan Lanka in his independent investigations. Prolonged serum deprivation alone can lead to cell rounding, detachment, and apoptosis, meaning that the observed effects in cell cultures could result from the artificial conditions themselves, rather than from any “virus.”

For example, a 1997 study on NIH-3T3 cells found a loss of viability and cell death due to serum starvation and antibiotic use:

Antiapoptotic effect of ras in the apoptosis induced by serum deprivation and exposure to actinomycin D

“The present study reveals that untransformed NIH-3T3 cells respond with a loss of viability to serum deprivation and also to the cytostatic drug actinomycin D. The loss of viability is associated with the appearance of cells showing the classical features of apoptosis (nuclear condensation, cell shrinkage).”

“NIH 3T3 cells will remain in the cell cycle in the presence of serum growth support, whereas in the absence of the serum growth support the cycle is arrested in G1 and, after a period of several hours, the cells undergo apoptosis. Constitutive expression of v-H-ras turns on important signals to stimulate simultaneously G1 progression and repress cell death during serum deprivation.”

https://pubmed.ncbi.nlm.nih.gov/9050009/

Similarly, a 1999 study on V79 cells noted cell death and detachment from both serum starvation as well as antibiotic use:

Effect of serum starvation on expression and phosphorylation of PKC-alpha and p53 in V79 cells: implications for cell death

“The effect of serum starvation on the expression and phosphorylation of PKC-alpha and p53 in Chinese hamster V79 cells was investigated. Serum starvation led to growth arrest, rounding up of cells and the appearance of new PKC-alpha and p53 bands on Western blots. Prolonged incubation (> or = 48 hr) in serum-deprived medium led to cell detachment and death. Moving cells to fresh medium containing 10% serum before, but not after, cell detachment reversed the changes observed in PKC-alpha and p53, and also prevented later cell detachment.”

“Our observation of cell death induced by prolonged serum starvation or by exposure to staurosporine or actinomycin D is in agreement with other studies. Serum starvation (Chou and Yung, 1997), staurosporine (Couldwell et al., 1994) and actinomycin D (Chou and Yung, 1997) have all been shown to induce cell death via apoptosis.”

https://pubmed.ncbi.nlm.nih.gov/9935181/

These studies demonstrate that serum deprivation alone can cause the same cellular damage attributed to “viral infection.” As noted earlier, various other variables—such as bacterial contamination or chemical exposure—can also produce this damage, none of which require the existence of a “viral” agent.

This highlights a critical flaw in virology: the reliance on effects that are not specific to a “virus” as supposed evidence of its presence.

Cytopathogenic effects are manufactured outcomes of laboratory manipulation, not observations of naturally occurring disease. Because CPE does not arise in nature and can result from a wide range of unrelated causes, it fails to meet the criteria for a valid dependent variable in experiments seeking to explain natural disease processes.

Its use as evidence for “viral” presence and causation reflects a departure from empirical science—substituting artificial artifacts and speculative inference in place of observed natural phenomena and testable, falsifiable hypotheses.

It is clear to those who understand natural science, the scientific method, and logical reasoning that cell cultures are a pseudoscientific setup. The literature is already rich with examples exposing the inherent flaws in this methodology.

However, it never hurts to add more evidence—especially when it comes directly from the published record. One particularly revealing case that further exposes this scientifically invalid practice involves what became known as the mirror cytopathic effect (mCPE), where cellular damage was observed even when no presumed “viral” material was introduced.

Thanks to the work of Vlail Petrovich Kaznacheev and colleagues in Russia during the late 1960s to early 1980s, we can drive yet another nail into the pseudoscientific coffin of virology by highlighting the nonspecific nature of its artificial, lab-created effects.

From the 1960s to the 1980s, Vlail Petrovich Kaznacheev—one of Russia’s leading medical scientists and founder of key research institutes—led numerous experiments to explore “non-contact” cell-to-cell communication.

In his 1979 paper Conditions controlling the development of distant intercellular interactions during ultraviolet radiation, Kaznacheev reported that as early as 1966, his team had observed that cultured cells (“detector” cultures), grown on quartz supports, could mirror the radiation-induced changes of nearby cultures exposed to extreme chemical or biological stress. This phenomenon was termed the “mirror” cytopathic effect (mCPE).

To investigate this “non-physical” communication, Kaznacheev’s team designed experiments focusing on the role of ultraviolet (UV) radiation. Their 1979 studies followed two main paths:

1. Reproduction of the CPE in a mirror detector culture exposed optically (but not physically) to a UV-irradiated radiating culture.
2. Investigation of mCPE in detector cultures pre-treated with minimal UV, then placed in optical contact with “virus-infected” radiating cultures.

Using Hep-2 (human laryngeal carcinoma) and FECh (human embryonic fibroblast) cells, separated by either quartz (which transmits UV) or glass (which blocks it), they found CPE occurred in 384 of 500 experiments—but only when quartz was used.

No CPE occurred through glass. In the second set of experiments, mild UV pre-treatment of the mirror cultures made it more susceptible to CPE when optically exposed to “virus-infected” cells—despite no “viral” material crossing between chambers.

This demonstrated that CPE could arise from light-mediated, “non-viral” interactions, not “infection.”

Kaznacheev concluded that stressed or dying cells—especially those under UV stress—emit signals that can trigger specific morphological degeneration in nearby cells, even in the absence of direct contact or “viral” material. This challenged the conventional assumption that CPE is exclusive proof of “viral infection.”

“The objects of the investigation were to study the role of uv radiation in distant intercellular interactions (DII) and the conditions for obtaining a “mirror” cytopathic effect (MCPE).

An extremal state of the cells in the radiating culture caused by uv-radiation was shown to induce a distant cytopathic effect (CPE) in an intact detector culture in optical contact only with it, reflecting the specific character of the morphological features recorded in the affected culture.

Preliminary uv-irradiation of the detector cells facilitates manifestation of the MCPE.”

In 1980, Kaznacheev’s group expanded their work to explore whether electromagnetic radiation—specifically in the UV spectrum—could serve a biological signaling function. They exposed tissue cultures to stressors such as “viruses” (Coxsackie A-13 and fowl-pest “virus”) or mercuric chloride.

Tissue cultures were chosen for their sensitivity and observable responses to cellular stress. When paired with healthy detector cultures—physically isolated but optically connected—the researchers found the same characteristic degeneration occurring in the mirror cultures.

Distant intercellular electromagnetic interaction between two tissue cultures

The existence of very weak intrinsic emission of radiation from biological objects (biochemiluminescence) is now generally accepted [1-4]. So far there have been few investigations aimed at determining the possible role of electromagnetic radiation in biological systems, although the possibility that biological objects can emit intrinsic radiation of different ranges has been demonstrated [5-7]. There is reason to suppose that electromagnetic interaction is a general principle of interchange of information among biological systems. Quanta with different frequency characteristics may perhaps be carriers of information.

Since 1966 the authors have studied the phenomenon of distant intercellular interaction due to electromagnetic radiation in the UV band [8-11]. The method of biological detection suggested by A. G. Gurvich has been used in our investigations to study the biological action of electromagnetic radiation in the biosystem.

Since we were interested to discover whether the electromagnetic radiation of cells performs a signal function, it was necessary to choose a state of the cells which could be clearly analyzed with the aid of the biological detector. A suitable object from this standpoint was a tissue culture infected with different viruses (Coxsackie A-13, the classical fowl pest virus — FPV) or treated with mercuric chloride.

In these cases the specific action of the viruses and mercuric chloride could be analyzed on the basis of their cytopathic action and immunologic changes. The experiments were planned so that the tissue culture infected with viruses or injured with mercuric chloride was the source of a specific signal, encoded in very weak radiation of the cells, and the intact tissue culture (not infected with virus) would serve as detector of this radiation.

In the cells of the intact culture (henceforward designated the “mirror” tissue culture), in optical contact with the affected tissue culture, all morphological features of the extremal states specifically characteristic of the corresponding agent, developed. These morphological features are henceforward described as the “mirror” cytopathic effect (CPE).

The team used primary human and chick embryonic fibroblast cultures, as well as transplantable monkey kidney tissue cultures. In each experiment, both chambers were equally bathed in nutrient medium to ensure the cells remained nourished and viable.

Controls were included to detect any spontaneous degeneration. Altogether, they conducted around 1,500 experiments with controls, carefully examining each for morphological changes.

This is taken from a long document. Read the rest here substack.com

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