PERTH GROUP COMMENTARY
ON THE DURBAN DECLARATION
12 August 2000
Below is the Perth group commentary on the Durban Declaration. This was
sent to the editor of Nature with the following covering note:
Dear Dr. Campbell,
Please find attached comments by my group to the Durban Declaration.
The reasons prompting this submission are two-fold. Firstly, the Durban
Declaration was a response to President Mbeki's decision to host a selected
panel of scientists to debate the HIV theory of AIDS in South Africa in May
and July this year. My group attended the second meeting and made an
invited presentation on "HIV Testing and Surveillance"
(www.deltav.apana.org.au/~vturner/aids). Your correspondent in South
Africa, Dr. Michael Cherry, was an observer at all proceedings over the two
days of the meeting, including the subcommittee which deliberated and then
resolved to perform experiments to prove or disprove the specificity of the
HIV antibody tests for proving HIV infection. This outcome was agreed to
by Professor William Makgoba of the Medical Research Council of South
Africa, Dr. Helene Gayle of the US Centers for Disease Control, as well as
Professor Barry Schoub and Dr. Caroline Williamson, both two South African
experts in virology. For some reason, news of this event was not conveyed
to the readership of Nature, although Dr. Cherry was also present at the
post-meeting press conference where this was made public. At the press
conference Dr. Gayle repeatedly said there was a need to get "back to
basics". Our attached comments document the scientific arguments we put to
the meeting which assisted the Panel in reaching its decision to conduct
these experiments. (Which are currently being designed in various centres).
Second, the Durban Declaration was presented by 5000 plus
scientists/physicians as their scientific rationale for upholding the HIV
theory of AIDS. Using data over the same time span we argue the contrary.
As President Mbeki himself observes, there are many scientists who, from
many angles, present scientific arguments questioning the HIV theory of
AIDS. Everyone acknowledges the generous contribution of space Nature has
provided in the past to address matters raised by Peter Duesberg. However,
my group's papers, including one published in Nature Bio/Technology in
1993, raise many questions totally removed from Duesberg. These concern
the basic tenets of the HIV theory including for example, the antibody
tests and HIV isolation. Such questions have never been addressed let
We realise that space is a constant premium but we would be most willing to
shorten this contribution. Alternatively, perhaps you might consider a
precis and, as with the Durban Declaration, make use of your website for
the bulk of the writing.
Fax +618 92241138
Voice + 618 92242500
On 13th of September we received the following Fax:
12 September 2000-09-14
Re: E Papadopulos-Eleopulos et al "Commentary-The Durban Declaration"
Thank you for submitting your manuscript, which we regret we are unable to
It is Nature's policy to decline a substantial proportion of manuscripts
without sending them to referees, so that they may be sent elsewhere
without delay. Decisions of this kind are made by the editorial staff when
it appears that papers are unlikely to succeed in the competition for
Among the considerations that arise at this stage are the pressure on space
in the various fields covered by Nature and the likelihood that the
manuscript would seem of great topical interest to those working in the
same or related areas of science. We believe that the arguments put
forward have been well rehearsed in the past and would be better suited to
an AIDS journal.
Sorry not to be more positive on this occasion.
Dr Richard Gallagher
Biological Sciences Editor
COMMENTARY THE DURBAN DECLARATION
Eleni PapadopulosEleopulos(1) Valendar F.Turner(2) John M.
Papadimitriou(3) David Causer(1) Barry Page(1) Helman Alfonso(4)
(1) Department of Medical Physics, (2) Department of Emergency Medicine, Royal
Perth Hospital, Perth, Western Australia; (3) Department of Pathology,
University of Western Australia. (4) Department of Research, Universidad
Metropolitana Barranquilla, Colombia.
For the HIV theory of AIDS to be accepted, evidence must exist which proves:
(1) As stated in the Declaration, "Patients with acquired immune deficiency
syndrome, regardless of where they live, are infected";
(2) The theory can account for all the phenomena for which it was put forward;
(3) Its predictions have been fulfilled.
Since by definition a patient is said to have AIDS only if he/she has a
positive antibody test, the only test routinely used to prove HIV
infection, it follows that all patients have a positive antibody test.
However, questions exist as to what the test means. In the antibody tests
some proteins which are said to be HIV proteins are reacted with patient sera.
According to Luc Montagnier, the leader of the team that claimed to have
discovered HIV seventeen years ago, the characterisation of proteins as HIV
proteins "demands mass production and purification [of the virus], it is
necessary to do that".(1) Ten years before, the principal and second authors
of Montagnier et al 1983 paper also stressed that to characterise a
retrovirus and its constituents one must purify the particles, that is,
isolate them from any other biological constituents.(2, 3) This has not
been done either by Montagnier or anybody else, a fact accepted by some of
the best known protagonists of the HIV theory.(4, 5) In fact, in 1997,
Montagnier acknowledged that the material which he and his colleagues
claimed to be "purified" HIV did not even have particles with "the
morphology typical of retroviruses".(1) Nonetheless, because some proteins,
including a protein of molecular weight 24,000 in this material reacted
with patient sera, they chose to call these HIV proteins, and the
antibodies, HIV antibodies. At present there is ample evidence that the
"HIV" proteins are cellular proteins(4, 6-8) Evidence also exists that AIDS
patients and those at risk have auto-antibodies as well as antibodies to a
plethora of infectious agents which cross-react with the "HIV" proteins.(6,
9, 10) In other words, whatever positive antibody test means it cannot be
considered proof for HIV infection. The fact that a positive antibody test
does not mean HIV infection is accepted by the test kits manufacturers: "At
present there is no recognized standard for establishing the presence or
absence of HIV-1 antibody in human blood.(11)
The HIV theory of AIDS was put forward to account for the high frequency of
some clinical and laboratory phenomena in gay men, IV drug users, and
haemophiliacs, none of which were new.
The main clinical phenomena were Kaposi's sarcoma (KS) and Pneumocystis
carinii pneumonia, the former constituting the basis for a relationship
between AIDS and retroviruses. At present everybody, including the CDC,
acknowledges that HIV plays no role, either directly or indirectly, in the
development of KS.(12, 13) The laboratory phenomenon was a decrease in T4
cells, determined by binding of the CD4 antibodies. It was postulated that
HIV infection lead to T4 destruction (Acquired Immune Deficiency, AID),
which in turn leads to opportunistic infections, S.
Thus, the foundation of the HIV theory is:
|Infection with HIV
|| T4 Destruction (AID)
Even if one assumes that the first step is proven, the theory cannot be
accepted unless the other two are also proven.
At present there is evidence that the decrease of T4 cells in blood is not
due to their destruction by HIV or any other factor, and that decrease in
T4 cells is not correlated with disease progression. "This article
discusses the importance of alterations in the CD4+ and CD8+ cell migration
in regulating blood lymphocyte levels and questions the extent of
virus-mediated CD4+ cell destruction";(14) "CD4+ T-cell lymphopenia is due to
both shortened survival time and a failure to increase the production of
circulating CD4+ T-cells";(15) or to the down-regulation of the CD4
molecule.(16) In other studies it was shown that, "CD4 [T4] cell counts were
not significantly associated with the risk of progression" to disease and
that "Along with other recent analyses and experimental developments these
conditions also suggest a need to re-evaluate current concepts about HIV
pathogens including the concept that a systemic depletion of CD4 T-cells is
the hallmark of the disease".(17) In fact, evidence exists which shows that
"low numbers of T4 cells was the highest risk factor for HIV infection",
that is, decrease in T4 cells is the cause and not the effect of "HIV
seroconversion".(18, 19) It may be of interest to note that as early as
1985, Montagnier knew that the immune deficiency in the AIDS risk groups
was not caused by HIV: "This [AID] syndrome occurs in a minority of
infected persons, who generally have in common a past of antigenic
stimulation and of immune depression before LAV [HIV] infection".(20) In
conclusion, a decrease in T4 cells is neither necessary nor sufficient for
disease to develop. This finding totally contradicts the HIV theory of
AIDS, that is, that HIV infection results in a decrease in T4 cells (AID)
which in turn results in S (diseases), and by itself is sufficient for one
to question the HIV theory of AIDS.
The main prediction of the HIV theory of AIDS was, that although AIDS was
first diagnosed in gay men, because AIDS was caused by a sexually
transmitted agent which like all other such agents is bidirectionally
transmitted, AIDS would rapidly spread throughout the heterosexual
population. One of the first scientists to publish data that this could
not be the case, at least in gay men, was Robert Gallo and his
associates. In 1984 he wrote: "Of eight different sex acts,
seropositivity correlated only with receptive anal intercourse...".(21) In
1986 Gallo wrote: "Data from this and previous studies have shown that
receptive rectal intercourse, for example, is an important risk factor for
HTLV-III [HIV] infection...We found no evidence that other forms of sexual
activity contributed to the risk".(22) This was confirmed in many other
studies including the Multicenter AIDS Cohort Study, (MACS) the best,
largest (about 5,000 men), and longest study which commenced in 1984 and is
ongoing.(23) In this, as well as other studies, it was shown that it is the
frequency of passive anal passive intercourse, not the number of partners
which is important in the development of a positive antibody test and
AIDS.(24-26) In a 1994 review of most, if not all the epidemiological
studies conducted in gay men, the authors concluded: "it can be said that
the cited reports yield convincing evidence that (1) unprotected
ano-genital receptive intercourse poses the highest risk for the sexual
acquisition of HIV-1 infection; (2) ano-genital insertive intercourse
poses the highest risk for the sexual transmission of HIV-1 infection; (3)
there is mounting epidemiological evidence for a small risk attached to
oro-genital receptive sex, biologic plausibility, credible case reports and
some studies show a modest risk, detectable only with powerful
designs; (4) sexual practices involving the rectum and the presence of
(ulcerative) STD facilitate the acquisition of HIV-1; (5) no or no
consistent risk for the acquisition of HIV-1 infection has been reported
regarding other sexual practices such as ano-genital insertive intercourse
and oro-anal sex...(8) the association of substance use with HIV infection
is probably the result of interaction, because substance use increases the
likelihood of practising ano-genital receptive
intercourse".(27) Unquestionably, to date, the best designed and executed
study in heterosexuals was conducted by Nancy Padian and her
associates. In 1987 they reported: "The total number of exposure to the
index case (sexual contacts with ejaculation) and the specific practice of
anal intercourse" were associated with the development of a positive
antibody test. The results from their long (ten years) prospective study
of heterosexual couples of whom only one partner of either sex was
antibody positive were published in 1997 where they reported that "no
seroconversions occurred among exposed partners".(28) According to one of
the best known HIV/AIDS experts, Jaap Goudsmit, for heterosexual "HIV
transmission" anywhere in the world, including Haiti, Africa, Thailand, "a
homosexual or anal factor seems to be required".(26) In other words, at
present there is ample evidence that sex plays an important role in the
acquisition of a positive antibody test and AIDS and the practice of safe
sex should form the basis for any effort in prevention. However, there is
no proof that AIDS is a bidirectionally sexually transmitted
disease. Unlike any other sexually transmitted disease, AIDS and a
positive antibody test, like pregnancy, can be sexually acquired but not
sexually transmitted. The difference is that while pregnancy can be
acquired by a single sexual intercourse, for AIDS to appear a very high
frequency of receptive anal intercourse over a long period is
necessary. AIDS is more like anal(29, 30) and cervical cancer.(31) The effect
is not the result of the act itself but its high frequency. However, as
with pregnancy, cervical and anal cancer, other factors may promote or
militate against the development of AIDS and a positive antibody test.
If a hypothesis cannot account for the phenomena for which was put forward,
and if its predictions are not fulfilled, then scientists have no choice
but to reappraise it.
1. Tahi, D. Continuum 5, 30-34 (1998).
2. Toplin, I. Spectra , 225-235 (1973).
3. Sinoussi, F., Mendiola, L. & Chermann, J.C. Spectra 4, 237-243 (1973).
4. Bess, J.W., Gorelick, R.J., Bosche, W.J., Henderson, L.E. & Arthur,
L.O. Virol. 230, 134-144 (1997).
5. Gluschankof, P., Mondor, I., Gelderblom, H.R. & Sattentau, Q.J.
Virol. 230, 125-133 (1997).
6. Papadopulos-Eleopulos, E., Turner, V.F. & Papadimitriou, J.M.
Bio/Technology 11, 696-707 (1993).
7. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. &
Causer, D. Continuum 4, 1s-24s (1996).
8. Arthur, L.O., et al. J. Virol. 69, 3117-24 (1995).
9. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. &
Causer, D. Curr. Med. Res. Opinion 13, 627-634 (1997).
10. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M.,
Causer, D. & Page, B. Curr. Med. Res. Opinion 14, 185-186 (1998).
11. Abbott Axsym system (HIV-1/HIV-2). Abbott
Laboratories, Diagnostics Division, Abbott Park. Illinois: United States
of America, 1988.
12. Beral, V., Peterman, T.A., Berkelman, R.L. & Jaffe, H.W. Lancet
335, 123-128 (1990).
13. Redfield, R.R. & Burke, D.S. Sci. Am. 259, 70-78 (1988).
14. Rosenberg, Y.J., Anderson, A.O. & Pabst, R. Immunol. Today 19, 10-7
15. Hellerstein, M., et al. Nat. Med. 5, 83-89 (1999).
16. Marodon, G., Warren, D., Filomio, M.C. & Posnett, D.N. Proc. Nat.
Acad. Sci. U S A 96, 11958-63 (1999).
17. Katzenstein, D.A., et al. NEJM 335, 1091-8 (1996).
18. Des Jarlais, D.C., et al. J. Acquir. Immun. Defic. Syndr. 6,
19. Nicolosi, A., et al. Epidemiology 1, 453-459 (1990).
20. Montagnier, L. Ann. Int. Med. 103, 689-693 (1985).
21. Goedert, J.J., et al. Lancet 2, 711-6 (1984).
22. Stevens, C.E., et al. JAMA 255, 2167-2172 (1986).
23. Kingsley, L.A., et al. Lancet i, 345-348 (1987).
24. Moss, A.R., et al. Am. J. Epidemiol. 125, 1035-47 (1987).
25. Palenicek, J., et al. J Acquir Immune Defic Syndr 5, 1204-11 (1992).
26. Goudsmit, G. Viral Sex-The Nature of AIDS (Oxford University Press,
New York, 1997).
27. Caceres, C.F. & van Griensven, G.J.P. AIDS 8, 1051-1061 (1994).
28. Padian, N.S., Shiboski, S.C., Glass, S.O. & Vittinghoff, E. Am. J.
Epidemiol. 146, 350-357 (1997).
29. Daling, J.R., et al. NEJM 317, 973-7 (1987).
30. Kondlapoodi, P. JAMA 248, 2114-5 (1982).
31. Reid, B.L., French, P.W., Singer, A., Hagan, B.E. & Coppleson, M.
Lancet 2, 60-2 (1978).