Perth Group Commentary on Durban Declaration August 11th 2000 - Submitted to Nature

Owned by Alex
Last updated: Apr 02, 2024
10 min read

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:

11/8/00

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 the writing.

 

Yours sincerely,

 

Eleni Papadopulos-Eleopulos
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
Perth
Western Australia

 

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 publish.

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.

Yours sincerely,

 

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 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 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 infections, S.

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 reappraise it.

REFERENCES

  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 (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 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).