What the Perth Group has argued
Papadopulos redox theory of cellular function papers
Papers and letters published in scientific journals
Monograph on mother-to-child transmission
Papers published in Continuum magazine
Papers published in the popular press
Papers/letters rejected by the scientific press
Selected email correspondence
A virus like no other
Oxidation, Montagnier and the Perth Group
Montagnier Nobel Prize 2008
The Parenzee Case
The House of Numbers
Questions and answers
Response to the NIH "Evidence" that HIV causes AIDS
Translations of the Perth Group papers
BMJ Online Debate
About the Perth Group
Perth Group at Virusmyth
The Perth Group on YouTube
PERTH GROUP COMMENTARY ON THE DURBAN DECLARATION August 11th 2000
REJECTED BY NATURE September 12th 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". 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 alone answered.
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
Fax +618 92241138
Voice + 618 92242500
On 13th of September we received the following Fax:
Dr E Papadopulos-Eleopulos
Department of Medical Physics
Royal Perth Hospital
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 limited space.
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 Papadopulos Eleopulos1 Valendar F.Turner2 John M. Papadimitriou3 David
Causer1 Barry Page1 Helman Alfonso4
1Department of Medical Physics, 2Department of Emergency Medicine, Royal Perth
Hospital, Perth, Western Australia; 3Department of Pathology, University of
Western Australia. 4Department of Research, Universidad Metropolitana
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 proteins4, 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
Thus, the foundation of the HIV theory is:
Infection with HIV --> T4 Destruction (AID) --> Syndrome (S).
Step 1 Step 2 Step 3
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 anal29, 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
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,
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
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 (1998).
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, 820-822 (1993).
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
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,