“As far as I'm concerned, and I hope this view is adequately represented, those who attempt to dispel the notion that HIV is the cause of AIDS are perpetrators of death. And I would very much
for one like to see the Constitution of the United States and similar countries have some means in place that we can charge people who are responsible for endangering public health with charges of endangerment and bring them up on trial. I think that people like Peter Duesberg belong in jail.” (Marc Wainberg, MD, chair of
this year's International AIDS Conference in Toronto)
At the beginning of the AIDS era, it was reasoned that if pathogen A ("HIV") leads to syndrome B (drop in absolute lymphocytes below 1000 cells/microliter and/or inversion of CD4/CD8-ratio of T-helper to T-suppressor lymphocytes), and syndrome B leads to condition C (opportunistic infections, Kaposi's sarcoma), then syndrome B (immune system collapse) necessarily occurs after A and precedes condition C (opportunistic infections, Kaposi's sarcoma). To think or show otherwise constitutes extreme AIDS denialism, because it denies the premises of the hypothesis. By contrast, those the spokespersons for the AIDS establishment pejoratively refer to as "denialists" are no such animals since we deny nothing. We question. And following the impeccable advice of the good (and almost godly) Dr. Einstein, in that "most important" activity, we never stop.
So perhaps those who really endanger public health are not Prof. Duesberg et al. but Dr. Wainberg (holder of drug patents and drug company research grants) and his fellow travellers, and they are the ones who deserve to stand before panels of stern judges.
For example:
Luc Montagnier et al. are AIDS denialists
AIDS denialism appeared for the first time when Luc Montagnier and his colleagues claimed in Nature (in 1986) that LAV replication (HIV's first name: Lymphodenopathy-Associated Virus), and its associated cytopathic effects (damage to T4 cells), only occurs when T4 cells are "activated:"
"....replication and cytopathic effect of LAV can only be observed in activated T4 cells. Indeed, LAV infection of resting T4 cells does not lead to viral replication or to expression of viral antigen on the cell surface, while stimulation by lectins or antigens of the same cells results in the production of viral particles, antigenic expression and the cytopathic effect (2).
In this logical construct, A (“HIV)” does not lead to B (immune suppression/collapse) to produce C (AIDS-defining illnesses), because A (“HIV) is not necessary (or present in the control non-infected cultures) to induce B (destruction of T-lymphocytes/immune collapse), because a chemical, PHA, induces the T-cells to become activated and sick in the absence of the virus, leading to a situation in which the cell culture is coaxed artificially into shedding 80-160 nanometer membrane-coated “viral-like particles,” reverse transcriptase” (RT), and other surrogate markers thought to be specific components of the "HIV virus.” To generate, and isolate "HIV" (A) from T-cell cultures, Montagnier et al., by their denialism suggested that "A" isn't even necessary, but chemical stimulation is essential (3-7).
Flossie Wong-Staal and Robert Gallo are AIDS denialists
Robert Gallo refused to attend this summer's Toronto International AIDS Conference because he wasn't invited as a keynote speaker. In an interview, he claimed that the conference was "a circus-like" affair devoid of basic science. Perhaps this comes as no surprise because in 1985, Flossie Wong-Stall and Robert Gallo published that:
"The association of Kaposi's sarcoma with AIDS deserves special mention. This otherwise extremely rare malignancy occurs predominantly in a restricted group, that is, the homosexuals, and can occur in the absence of any T-cell defect in the patients" (8).
Wong-Staal and Gallo in their statement in Nature quoted above, claimed that the "HIV=AIDS" chain of events does not happen such that A (“HIV”) leads to B (immune collapse), which leads to C (AIDS-indicator diseases: OI’s or Kaposi’s).
Instead, Staal and Gallo suggested that the formation of Kaposi's sarcoma (C) occurs without T-cell depletion and immune collapse (A leads to C without B). Therefore, they are AIDS denialists.
Gallo and his colleagues also reported that:
"the expression of HTLV-III ("HIV"s second name-Human T-cell Lymphotropic Virus number III) was always preceded by the initiation of interleukin-2 secretion, both of which occurred only when T-cells were immunologically activated" with PHA (9).
Therefore, both Gallo's and Montagnier's groups advocated a similar type of AIDS denialism, and both groups published that mitogenic stimulation and activation (of T-cells) in the absence of "HIV," can induce the same cytopathic effects as healthy, non-infected cultures that are treated with sera or cells derived from "AIDS" patients, only when mitogens such as PHA are present.
Nobelists, Howard Temin, and former NIH head Harold Varmus advocated AIDS denialism
It is widely appreciated amongst "HIV=AIDS proponents that reverse transcriptase (RT) is an indication of the presence of retroviruses, and particularly "HIV." However, Nobelist, Howard Temin who discovered RT, and Nobelist and former NIH head Harold Varmus, claimed that reverse transcriptase (RT) is a normal protein found in the uninfected cells of yeasts, insects and mammals (11). More recently, other AIDS denialists have claimed RT is important for telomere replication at the tips of normal chromosomes, and "has nothing to do with retroviruses as such." Nowadays, this denialism has led the biotech industry to perpetuate the notion that RT is not specific for retroviruses. For example, the non-specificity of RT is known in the form of market magazines concerning biotechnology stocks (12, 13). Claiming as Temin and Varmus did, that RT is a non-specific characteristic of A ("HIV" virus) thus constitutes a form of AIDS denialism at the cellular level, and indeed denies the mechanism of "HIV" integration into the host cell's genome.
Additional examples of true AIDS denialism from mainstream HIV/AIDS workers and establishment cathedrals are contained in the PDF file of an unabridged version of this article that can be read in its completely referenced entirety, here.
Andrew Maniotis, is a program director in the Cell and Developmental Biology of Cancer unit of the
Department of Pathology, Anatomy and Cell Biology, and Bioengineering, College of Medicine, University of Illinois at Chicago.
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