I am responding to your recent article in the hopes that this will initiate a discussion but, in the absence of that, to correct the record to Fabio Franchi and the many other recipients of this email, and to raise some questions about your paper and your theories. I sincerely would like answers.
I should point out that I have for more than a decade been persuaded by the Perth Group's non-existence of HIV arguments. Your Oxidative stress arguments are persuasive, although there are some problems in the context of HIV which I'll describe below. But I'm not at all persuaded by your arguments about semen.
First the outright errors of fact:
Rethinking AIDS has not ignored people who do not subscribe to the passenger virus theory. Please note the following:
The president of RA (me) does not subscribe to the theory. And this has been documented for over a decade. Please stop mis-stating my views.
I do not believe that it is my right and it is certainly not my desire to attempt to impose scientific viewpoints on the board or membership of RA. Knowing there are a diversity of views on the issue of virus existence there is no point trying to create a consensus statement on this topic.
I have never ignored or censored Neville. I have posted a link and commentary to virtually everything he has written in recent years on aras.ab.ca. I consider him one of the heroes of the movement. I have often consulted with Neville and always found him cordial and cooperative.
I have not ignored Djamel Tahi but until a couple of months ago I had no contact information for him. As soon as contact was established (January 2010) RA published an article by him on the front page (it is still there).
Regarding the three theories of AIDS:
Obviously I agree that the HIV theory of AIDS exists. No comment there.
From a perspective of AIDS, Duesberg's theory is virtually identical to yours. Duesberg says that drugs, malnutrition and exposure to foreign blood products cause AIDS. So do you. You have identified oxidative stress as a common denominator, which is important but the only additional factor you introduce is semen.
The 'passenger virus' (HIV in Duesberg's theory) is irrelevant to AIDS. It is the cause of irrelevant antibodies according to that theory, not the cause of AIDS.
But, what is AIDS? I am certainly glad that this time you have attempted to define the term but I have some questions:
Why have you ignored AIDS in Africa?
You mention low T4 (CD4) cells. Do you consider these AIDS?
Does HIV have any relevance in your definition? For example, is Kaposi's Sarcoma always AIDS? Is Tuberculosis always AIDS? PCP? Or are they only "AIDS" in your view with HIV antibodies?
If you believe that HIV is not necessary for AIDS how can you talk about an "AIDS era".
If you do not believe that HIV is necessary (but maybe it increases the risk) then hasn't AIDS existed for millenia?
I agree that a large population of HIV+ people will probably have more disease than HIV- but this does not mean that the HIV+ test has useful prognostic value for an individual. You seem to be ignoring the many healthy, HIV+ people with no indications of disease. What is your message to them? Should they be concerned? Have you considered the psychological impact of saying that, "there is no denying that a positive antibody test, at least in the AIDS risk groups, increases the probability of the presence or the development of AIDS". Many people will take this as applying to an individual (them). Is your statement intended for individuals or just for groups?
What are "AIDS risk groups"? Do you define them the same way as the mainstream? If not, could you please define what they are. For example:
Do you consider all gay men a risk group? Or only those who indulge in anal sex? Or only those who are highly promiscuous? Or only those who use poppers? Or certain combinations?
Do you consider all drug abusers a risk group? Or only those who use IV drugs? Are clean needle users still in a risk group?
Are black Africans a risk group for AIDS?
It is extraordinarily important for you to define this term because, in the absence of clarification, your user of the term "AIDS risk group" will have to be taken to mean what the CDC and WHO think it means.
When you say that "All 'HIV' experts accept that 'HIV' positive individuals and those at risk have auto-antibodies." do you mean all HIV+ people have auto-antibodies and all those "at risk"? Or just some? Do you mean that the presence of auto-antibodies is a better risk indicator than a positive HIV test? Are there standardized tests for this, and do you encourage people to take them?
You state that, "The epidemiological evidence of the last 25 years shows that an "HIV positive" test can be sexually acquired but cannot be sexually transmitted. This single fact proves that whatever the test may signify it cannot be infection with a sexually transmitted agent." but:
I addressed the evidence you provided and it showed mainly that a high level of anal sex was associated with a higher risk of HIV seropositivity in healthy men, not AIDS.
And no risk co-factors were considered (like drug use, anal douching, other sexual practices such as fisting, and so on)
Clearly your semen hypothesis is a theory not a fact, as you describe it.
You remind us that, "Last year, when [the] UN declared the end of heterosexual AIDS [a bit of an exaggeration as they excluded Africa], Michael Ellner was worried that sooner or later there will be a backlash against the gay community. If [t]his occurs then, according to our theory, it will have no scientific basis."
No, your theory blames anal sex, by itself, with no co-factors such as drug use, for AIDS. If that theory was to be widely accepted there could be an enormous backlash against gay men as their sexuality would be seen as the basis for a worldwide epidemic that killed millions. For you to promote this theory so heavily with such limited evidence is very dangerous.
I don't wish to defend the passenger virus theory but Duesberg very clearly stated that HIV-antibodies were related to the dose of, for example, Factor VIII. He explained this by hypothesizing that, in a large population, the more exposures, the greater the risk of an HIV infection. Therefore your hypothesis that dose of drugs or dose of blood products would distinguish the oxidative stress-causes HIV-seropositivity theory from the passenger-virus-associated-with-risky-activity theory is not true.
The study that convinced me that the passenger virus theory was not true was the Bruneau study of IVDUs published in 1997. This showed that clean needle exchanges increased the rate of HIV seropositivity. This was a good way to separate out the passenger virus from the drug. This showed two things against the passenger virus theory:
Clean needle exchange users used more drugs implying that the drugs were causing the HIV seropositivity (making the passenger virus unnecessary to explain seropositivity).
Clean needle exchange users would have been less exposed to passenger viruses and therefore should have had lower seropositivity risk if the passenger virus theory was true. But the opposite was true.