Re: Re: Re: The non-existent knobs on "HIV" particles 23 July 2004
Previous Rapid Response Next Rapid Response Top
Christopher Tyler,

Send response to journal:
Re: Re: Re: Re: The non-existent knobs on "HIV" particles

Christopher Noble misses the two primary points of my previous post. The first point being, the Perth Group's Oxidative Stress theory's predictions have been validated since those predictions were put forth. The research by Stanfard University was quoted as showing that higher levels of oxidation (decreases in GSH in particular) was associated with an increased risk of ill health and death.

"Clinical studies presented here directly demonstrate that low GSH levels predict poor survival in otherwise indistinguishable HIV-infected subjects. Specifically, we show that GSH deficiency in CD4 T cells from such subjects is associated with markedly decreased survival 2-3 years".

In other words, it's the depleted GSH that is the critical factor here. This is what the oxidative stress theory predicts. In fact, they go on to say, "GSH deficiency has long been known to be clinically dangerous in man and in experimental animals. T cell function (16-18, 30-32) and viability (33-35), are markedly impaired in GSH-depleted T cells."

For 'HIV' to account for the decrease in GSH levels it would need to be present in sufficient quantities to have profound oxidative properties. That is, it would need to infect sufficient numbers of T-cells to deplete their GSH reservoirs. Yet 'HIV' is said to infect far too cells to do this. As Peter Duesberg writes:

"there is very little detectable virus in AIDS patients. Fewer than 1 out of every 10,000 of the host's T-helper cells are actively infected by HIV even during AIDS;... Fewer than 1 in 500 of a host's T cells contain even dormant HIV which can only be found by isolating these cells from the body and stimulating them artificially..."

Even Montagnier couldn't find any virus in his 'purified' gradients. One would logically have to look at much stronger factors which would decrease GSH levels throughout the body. Again, Peter Duesberg writes:

"In 1983, two dozen of America's leading AIDS investigators including Friedman-Kien, Curran, and CDC worker Harold Jaffe, later director of the CDC's HIV/AIDS Division, had conducted extensive epidemiological studies which revealed overwhelming drug use, including nitrite inhalants, cocaine, and amphetamines by all homosexual AIDS patients studied (Table 2) (Jaffe et al., 1983)."

That these chemicals when taken at recreational doses saturate the body with oxidizing molecules is again discussed by Duesberg:

"A typical daily dose of 1-2 g of cocaine (10, 67), or heroin (126) or amphetamine (118) consists of about 1021 molecules, or 10^7 molecules for every one of the 10^14 cells of the human body."


"Nitrite inhalants react with all biological macromolecules, mutating and inactivating DNA and RNA, diazotizing proteins, killing vitamins and oxydizing hemoglobin to inactive methemoglobin (26). At the recreational dose of 1 ml per day (26, 130, 131) the user introduces about 10^21 molecules into the lungs, or 10^7 molecules for every cell in the human body enough for abundant toxicity. Under these conditions nitrites are cytotoxic and immunotoxic in animals and humans (130, 132)."


"The FDA also limits nitrites as food preservatives to less than 200 ppm (parts per million), because of direct toxicity and because 'they have been implicated in an increased incidence of cancer' (134)"
(Peter Duesberg and David Rasnick; The Drug-AIDS Hypothesis)

As Christopher Noble also points out, opportunistic microorganisms require reducing equivalents for division and survival which they leach from the host. It's known that men who began getting sick and those at risk had many infections (and often repeated infections) by many infectious agents. Drugs such as Bractrim were often used to treat many of these, further contrinuting to oxidative stress. That these infections would increase oxidation, in addition to the ubiquitous use of other (recreational) oxidising agents further argues in favor of the Oxidative Stress theory of AIDS.

The second point I made was, given that depleted GSH levels predict increased death rates, why is a drug like AZT being used to 'treat' people with depleted GSH levels? And, given that GSH levels predict survival, why would a non-sick person be given an agent which would reduce his GSH levels? And, why are drugs including AZT given to infants and children, 'some at higher than usual doses' at state run orphanages given that depletion of GSH 'predict decreased survival'?

I note that Christopher Noble failed to address these critical issues.

Chris Tyler

Competing interests: None declared