Alexander H Russell,
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Nicholas Bennett stated: "The fact that HIV infection precedes a CD4 T cell decline that is not seen in any other human condition is proof enough. It isn't even required that HIV directly kills the T cells, even though it does."
Until Bennett can clearly describe the precise mechanism by which 'HIV' destroys cells he is in no position to state that it does so - this is pure speculation.
Moreover, 'HIV' is invariably found in people with many other different kinds of antibodies due to concurrent infections with other pathogens: how do we know that one these is not responsible for the killing of T 4 cells? For instance: reactivated herpes viruses are highly cytotoxic. Has Bennett ever found evidence of 'HIV infection' in an individual with no other pathogens present? I very much doubt it. What we are calling 'HIV' is in fact merely an endogenous marker for other pathogens.
It is not a "fact that HIV infection precedes a CD4 T cell decline" but mere supposition because there is no such activity as 'HIV infection' to begin with so Bennett's statement is simply an absurd assumption and has no scientific foundation whatsoever. How can an endogenous epiphenomenon ('HIV') be an 'infections' agent in the first place?
What evidence does Bennett have that 'HIV' is destroying T cells by 'infection'? There is no empirical evidence cited in a reference paper for this hypothetical assumption: it is no more than speculation, supposition and wishful-thinking on Bennett's part.
Harvey Bialy, former Editor-at-Large for Nature Biotechnology and Research Editor of Bio/Technology, asked Dr. Jerold Lowenstein, of the University of California Medical Center, San Francisco, at the symposium, 'The Role of HIV in AIDS: Why There is Still a Controversy' (The Pacific Division of the American Association for the Advancement of Science) on the 21st of June,1994:
"You made the statement that HIV replicates in and destroys t-cells. This is the crux of the entire debate. What is your evidence?…What is your evidence that HIV is destroying t-cells by infection? I would love to see it. I've been waiting ten years for it."
As entirely expected, there was no response from Dr. Lowenstein.
In the late 1980s Luc Montagnier admitted that there was no evidence for 'HIV' directly killing T cells. By April 10th, 1990, Montagnier explained to a researcher colleague that the cell deaths in cell cultures containing 'HIV' were caused by a contaminating mycoplasma. When that was eradicated, using doxycyline, the cell killing stopped despite the fact that the cultures contained 'HIV'. This was clear evidence that this 'strain' of 'HIV' - which had previously been considered cytotoxic - was, indeed, harmless.
It is interesting to consider how many other examples in laboratories throughout the world have observed similar 'cell killing' strains of 'HIV' which were in fact due to mycoplasma contamination. When Dr. Shyh-Ching Lo infected four silver leaf monkeys with this same mycoplasma they all developed 'AIDS' like symptoms in short period of time and died. They were not 'infected' with 'SIV'.
In conclusion, I advise Bennett to read the following by The Perth Group:
A CRITICAL ANALYSIS OF THE HIV-T4-CELL-AIDS HYPOTHESIS by Eleni Papadopulos-Eleopulos,1 Valendar F.Turner,2 John M. Papadimitriou,3 David Causer,1 Bruce Hedland-Thomas,1 & Barry Page1 1: Department of Medical Physics, 2: Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia; 3: Department of Pathology, University of Western Australia.
The data generally accepted as proving the HIV theory of AIDS, HIV cytopathy, destruction of T4 lymphocytes, and the relationship between T4 cells, HIV and the acquired immune deficiency clinical syndrome are critically evaluated. It is concluded these data do not prove that HIV preferentially destroys T4 cells or has any cytopathic effects, neither do they demonstrate that T4 cells are preferentially destroyed in AIDS patients, or that T4 cell destruction and HIV are either necessary or sufficient prerequisites for the development of the clinical syndrome.
Competing interests: None declared