Why There is Still an HIV Controversy

*NO'v 16 '93 01: 471 ADARC FP. 6

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The perceived need to validate the direct causation
theory generated an enthusiastic reception for any research
that seemed to validate the premise that HIV is present in
quantity in the bodies of AIDS sufferers. For example,
research by Panteleo et al. employed the PCR technique to
locate relatively high concentrations of HIV sequences in
some AIDS patients, particularly in lymphoid tissues [4].
On this basis, the authors concluded that HIV infection is
"active and progressive even when... the patient is
experiencing clinical latency." However, replicatiozw
competent virus was not in fact quantitated in these studies
and the PCR technique cannot distinguish between such virus
and viral fragments. In our opinion, these findings merely
reflect the well-established role of lymph nodes in
sequestering virus prior to elimination rather than it
serving as a reservoir of infection.
If Drs. Gallo and Fauci really meant what they said
publicly at the latest NIH conference, as quoted above, then
such efforts to maximize the quantity of HIV present after
the primary infection seem pointless. Immune system damage
and other AIDSt-defining conditions can be attributed to HIV
even when no HIV is present in the body at the time of the
damage or disease occurs.
But how do we know that HIS causes AIDS at all? The
scientific community was promised several years ago an
authoritative paper proving that HIV is the cause of AIDS
[11], but what has appeared instead is ridicule of the
dissenters [13] and inadequately controlled epidemiological
studies of specific populations [26, 27]. It is concededly
possible for a pathogen to cause a disease even though the
mechanism is unknown, but when determined efforts by armies
of researchers have failed to find a direct physical cause,
and the research establishment has turned to speculative and
unfalsifiable alternatives, it is time to take a second look
at the other evidence that has been relied upon to establish
causation. When we do look at the evidence, here is some of
what we find:
1. There is no satisfactory animal model. Chimps can be
productively infected with -7+ V, but they do not develop AIDS
[lL-13]. It is claimed, however, that another retrovirus
(ShIV) causes an "AIDS-like disease" in macaques. We doubt
that 51lV disease is truly "AIDS-like" in the crucial sense
of causing immune system collapse many years after the
primary infection, when it is present (if at all) only in
very low titres [14, 193. In any case, that so many 1*IV
believers have accepted as proof of HI1V causation the fact
that a different virus causes a different disease in animal
subjects demonstrates only that the research community has
been infected by a powerful will to believe.