Re: More on Oxidation – the primary cause for AIDS and “HIV” 2 February 2005
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Nicholas Bennett,
Infectious Disease Postdoc/Clinician
Deparment of Pediatrics, University Hospital, Syracuse, NY

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Re: Re: More on Oxidation – the primary cause for AIDS and “HIV”

In reply to the Perth Group.

The cause of their "oxidative status" is simply rapidly cycling T cells, in response to chronic HIV infection.

I am not aware at all that the very same kit (provided by the same manufacturer) is interpreted differently in different countries. The "same" test may of course be manufactured in different ways by various companies.

HIV isolation is not the only way to ensure detection, since culture will only work if an entity is capable of replication.

It is the same reaction in some culture detection methods (others use RT-activity) but the reaction is of course reversed! To most people, being able to detect antibodies from the host AND antigen from cultures from the host is highly indicative of an infection. Most people clearly do not include the Perth Group!

Since the sequences detected in viral load are those of HIV, by definition viral load IS good evidence for ongoing viral replication. The Perth Group themselves have shown that antivirals inhibit HIV replication. In their paper "A Critical Analysis of the Pharmacology of AZT and its Use in AIDS " they cite literature showing reasonably well that the percentage of cells containing HIV-DNA does not change under antiretroviral therapy. However, they don't compare the situation with UNTREATED HIV patients, in which case the percentage of HIV-DNA containing cells increases [1]. Additionally, un-integrated DNA (a true measure of active HIV replication, as opposed to the more static proviral DNA load) decreases significantly while on therapy [2]. Rather ironically the Perth Group's AZT critique appears to support it's use as an antiretroviral.

In response to their questions:

Q1 Does not make sense, since "oxidized tissues" does not necessarily equate to increased SH levels. However it does appear that cellular redox may be affected, if they want to use the correct terminology. A qualified yes.

Q2 SH levels only predict survival because...

Q3 SH levels are associated with low CD4 T cell counts, and CD4 T cell counts predict survival. So yes on both counts, but since HIV causes a loss of CD4 T cells due to rapid cycling this doesn't mean HIV doesn't cause AIDS. SH levels alone do not predict much since in the absence of HIV infection.

Q4 HIV can be detected in culture without any use of oxidants and doesn't require "antioxidants" to be inhibited. Most tellingly, since many seem to consider AZT as an oxidizing agent, it seems ironic that AZT inhibits HIV replication in culture of non-stimulated T cells [3] The answer is no on both parts. Please note this data is over 15 years old - one wonders if the Perth Group chose to ignore it during their extensive literature searches. It was the earliest paper I found in the single PubMed search I undertook to confirm this, so was hardly difficult to discover.

Q5 I have not seen data looking directly at SH levels and viral load, but since SH levels correspond to rapid T cell cycling in response to HIV, one might agree that this could happen. Logically, yes.

Since the answers to Q 1 through 5 are not all yes, the Perth Group's conclusion does not follow. In fact, it would not follow anyway since they do not rule out the alternative possibility that HIV is causing the raised SH levels.

I'm surprised that the Perth Group state that "scientific thought does not count" when all they have provided to the world of HIV/AIDS research is opinions and scientific thought. One clearly has to add caveats to a dogmatic statement e.g. "HIV replicaton requires stimulation in some cell lines but not all". The caveat neatly destroys their hypothesis that stimulation is required for HIV expression - perhaps that is why they choose not to use it. Another would be "SH levels correlate with progression to AIDS, but perhaps because they are linked to CD4 T cell count which is itself independantly linked to AIDS". The loss of CD4 T cells makes rather more immunological sense than a non-specific affect on global cellular redox.

Perhaps the Perth Group can return the favour by responding to the following questions:

Q1 Why should a sexually transmitted disease be expected to be equally bi-directionally transmitted? There is no reason to assume this to be the case, especially considering the animal data [4], the fact that a male innoculum is far larger than a female's, and the fact that homosexual males are a largely sexually distinct risk group.

Q2 Why do they say that Montagnier failed to distinguish retroviral RT from mitochondrial DNA polymerase, when his 1983 "isolation" paper clearly states the opposite?

Q3 Can they show that individuals treated with chemotherapy and "other oxidizing agents" develop a progressive, specific decline in the single subset of CD4 T cells which is reversed by the addition of nucleoside analogue (in the case of HIV, RT inhibitor) medications?

Q4 Do they accept the National Cancer Institute's statement that Kaposi's Sarcoma is massively increased in frequency in immunosuppressed people?

Q5 Do they accept that a RT activity level in a culture spiked with virus compared to an uninfected culture is therefore due to the prescence of the virus as per the method of Potts? [5]

Q6 If the anti-HIV antibodies are non-specifically induced and are caused by the same thing that causes AIDS, why does lower anti-HIV antibody levels correlate with worse progression? [6]

Q7 Why does HIV-specific RNA levels correspond to the rate of CD4 T cell loss? [7]

Q8 If non-HIV stimuli cause spontaneous antibody, RNA and antigen formation coincident with CD4 T cell decline, what possible genetic mechanism can explain this spontaneous appearance in a subset of host cells?

Why not consider an infectious retrovirus?

Nick Bennett

1. Cone et al AIDS 12(17) 1998 p2253 "Levels of HIV-infecte­d peripheral blood cells remain stable throughout the natural history of ­HIV-1 infection"

2. Ibáñez A, Puig T, Elias J, Clotet B, Ruiz L, Martínez M-A. Quantification of integrated and total HIV-1 DNA after long-­term highly active antiretroviral therapy in HIV-1-infected patients. AI­DS Jun 18;13;1045-1049

3. Smith et al J Virol. 1987 Dec;61(12):3769-73. "Resumption of virus production after human immunodeficiency virus infection of T lymphocytes in the presence of azidothymidine."

4. Portis et al J Virol. 1987 Apr;61(4):1037-44. "Horizontal transmission of murine retroviruses."

5. Potts 1990 "Mini reverse transcriptase (RT) assay", p103-106 in Aldovini and Walker: Techniques in HIV research.

6. Munoz J Acquir Immune Defic Syndr. 1988;1(4):396-404." Predictors of decline in CD4 lymphocytes in a cohort of homosexual men infected with human immunodeficiency virus."

7. Lyles et al J Infect Dis. 2000 Mar;181(3):872-80. "Natural history of human immunodeficiency virus type 1 viremia after seroconversion and proximal to AIDS in a large cohort of homosexual men. Multicenter AIDS Cohort Study."

Competing interests: None declared