Perth Group's open letter to Professor Jean Umber concerning his
article 'What if HIV was simply a natural sign of cellular death
(apoptosis)' posted by Crowe on his ARAS website, '(copyright 2007 – Jean Umber and the Alberta Reappraising AIDS Society)' – which is to say, these ideas belong to Jean Umber and David Crowe
May 24th 2010
Dear Professor Umber,
we would like to thank you for your offer to financially contribute to
the Parenzee hearing. Also to point out that, regrettably, our
exchange of information regarding antiretrovirals was very brief.
There are two reasons for this.
Our interest in antiretrovirals is secondary. AZT and
nevirapine were exceptions. We performed a detailed analysis of
these drugs at the request of President Mbeki.
we have been necessarily distracted by dissident politics at the
expense of science.
our attention was drawn to a posting of yours entitled "What if HIV was
simply a natural signal of cellular death (apoptosis)?" on Crowe's
website, "(copyright 2007 – Jean Umber and the Alberta
Reappraising AIDS Society)".
by an earlier contribution of yours: "Why did HAART improve the
prognosis of AIDS" (translated from the French by you and "edited by
David Crowe", it is obvious that you are fully aware of our work. Since
(a) professes to be our leader;
not long before your posting we sent him a summary of our work and
asked him to post it on the RA website. Although he accepted that
our summary was factual, he declined to publish it on the grounds we
were seeking priority.
This being the case you must have known that we:
the first to put forward the hypothesis and present supporting
scientific evidence that the ""HIV" particles and proteins are nothing
more than "non-viral material altogether" induced by agents to which
the AIDS patients and cultures are exposed…" And that both
apoptosis and the "HIV" particles are induced by the same
mechanism: oxidation in general and myosin SHs in
particular. The latter will lead to myosin-actin interaction,
budding and ultimately to particles ("HIV") release. Excessive
oxidation, including "endogenous forming of peroxynitrates" is the
result of the many oxidising agents, including nitrites, to which the
patients belonging to the AIDS risk groups are exposed.1-3
were the first to show that both the viral load and the antibodies have
nothing to do either with "HIV" or even the "famous microvesicles"
released by lymphocytes. 4-8
the first to put a unifying drug theory of AIDS (Michael Cullen and
John Lauritsen preceded us in regard to AIDS in gay men) and to show
"that the real cause of AIDS" is the cellular oxidation induced by
drugs and semen to which these patients are exposed.7 9-12
shown that AZT cannot act as a DNA chain terminator. To perform
such a role the drug must enter the cell and be triphosphorylated in
the presence of reducing equivalents. However the cells of the
AIDS patients are oxidised and in addition the drug itself is
oxidising, which means it cannot be triphosphorylated and this is
exactly what the evidence shows.
have shown that AZT toxicity, including inhibition of DNA synthesis, is
the result of its oxidative nature: We wrote: "At present,
evidence also exists which shows that AZT is rapidly reduced by
compounds containing sulphydryl (-SH); that is, AZT oxidises the
–SH groups. Ample evidence also exists which shows that
oxidation in general (and of –SH in particular) and decreased
levels of ATP may lead to many laboratory and clinical abnormalities,
including wasting, muscular atrophy, anaemia, damage to the liver and
kidney, decreased cellular proliferation, cancer and
immunodeficiency. Since patients who are at risk of AIDS are
exposed to many oxidising agents and are known to have low –SH
levels one would expect AZT to have particularly toxic effects in these
individuals – and the sicker the patient the more toxic the
drug. That this is the case was accepted by researchers from the
National Cancer Institute, Wellcome Laboratories and Abbott
Laboratories as far back as 1988: 'Azidothymidine, however, is
associated with toxicities that can limit its use…These
toxicities are particularly troublesome in patients with established
AIDS; the use of azidothymidine is often limited in this
population'. Despite these caveats it is possible that, if a
thymidine analogue is to be administered to patients with AIDS or to
those at risk, at least part of its toxicity may be eliminated by
substituting the 3'-OH group with a –SH-group instead of an azido
(ºN) group. Yuzhakov et al have performed such experiments
and shown that the resulting compound inhibits 'HIV RT'".6
In other words, in our opinion, to decrease the toxicity of the
AZT types of drugs they should be modified and transformed from
oxidising to reducing agents. It appears, as you have shown in
your elegant work, that the "HIV" experts may have done exactly this
were therefore unpleasantly surprised that none of our original work
was mentioned, even once, let alone that it was attributed to others.
Eleni, Val and the Perth Group
1. Baranchila Conference.
2. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Oxidative stress, HIV and AIDS. Res Immunol1992;143:145-8.
3. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D. The Isolation of HIV: Has it really been achieved? Continuum 1996;4:1s-24s.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Stewart G, Causer
D. HIV antibodies: further questions and a plea for clarification. Curr Med Res Opinion 1997;13:627-34.
5. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Page BA. HIV antibody tests and viral load--more unanswered questions and a further plea for clarification. Curr Med Res Opinion1998;14:185-6.
Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D,
Alphonso H, Miller T. A critical analysis of the pharmacology of AZT
and its use in AIDS. Curr Med Res Opinion 1999;15:1s-45s.
7. Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation caused by the risk factors the primary cause? Med Hypotheses 1988;25:151-162.
8. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Is a positive Western blot proof of HIV infection?Biotechnology 1993;11:696-707.
Papadopulos-Eleopulos E, Page BA, Causer D, Turner VF, Papadimitriou
JM, Alfonso H. Would Montagnier please clarify whether HIV or oxidation
by the risk factors is the primary cause of AIDS?Med Hypotheses 2006;67:666-8.
Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Causer D.
Factor VIII, HIV and AIDS in haemophiliacs: an analysis of their
relationship. Genetica 1995;95:25-50.
Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Hedland-Thomas
B, Causer D, Page B. A critical analysis of the HIV-T4-cell-AIDS
hypothesis. Genetica 1995;95:5-24.
12. Papadopulos-Eleopulos E. Looking back on the oxidative stress theory of AIDS. Continuum 1998;5:30-35.