Infectious Disease Postdoc/Clinician
Department of Pediatrics, University Hospital, Syracuse NY
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In response to the Perth Group:
I find no evidence that suggests that semen, nitrite inhalants, or factor VIII are "oxidative". I think Mr Whitehead gave some evidence that opiods can affect cellular redox but this does not mean that they are oxidiative in the chemical sense. Malnutrition itself may not lead to "oxidation" (whatever that means - spontaneous combustion?) but it will of course lead to reduced intake of antioxidant nutrients which will perhaps lead to a reduced ability to deal with other stressors which may themselves be the cause of altered cellular redox.
I see no evidence therefore that AIDS patients are exposed to cellular oxidizing agents above and beyond non-AIDS patients.
The main predictions of the HIV/AIDS theory are that:
HIV serology should precede AIDS. HIV serology should predict HIV detection via other means (e.g. culture, PCR, antigen testing). Pharmacological intervention against the virus should inhibit the viral replication in vitro and in vivo, and result in restoration of the immune dysfunction seen in AIDS and pre-AIDS complex patients. HIV serology should, obviously, appear to be transmissible and associate with the individuals and risk groups associated with AIDS. All of these are true and have been discussed here before - in order for the Perth Group to maintain their oxidative stress theory they have had to concoct terribly convoluted explanations for the serology and culture methods, when Occam's Razor dictates that the simplest explanation is most usually the correct one.
One ommission made in the Oxidative theory of AIDS is that those with oxidative stress but without HIV should get AIDS. This isn't the case.
The argument that HIV requires oxidation for activation is a non- starter, although required by the Perth Group to explain the point above. This has been previously addressed here and is based on a superficial and flawed analysis of the literature, and generally ignoring evidence to the contrary. I would readily admit that IF it were the case that there was (a) evidence that HIV were endogenous and (b) it required oxidative stress for activation and (c) oxidative stress were a better predictor for AIDS than anything else it would make sense. It would also fit with much of the other literature out there (since nothing in the mechanism of how HIV causes AIDS would need to be altered). However the evidence is that HIV is (a) not endogenous (b) doesn't require cellular "oxidation" (again, whatever that means) to be activated and (c) oxidative stressors, or any kind of stressors associated with AIDS risk groups, are confounding factors.
The other point is that cellular redox appears to be a side effect of the immune activation and rapid cellular turnover seen in AIDS, and that by merely providing antioxidants one is treating the symptom and not the cause. I think that a two-pronged approach may be necessary.
Ironically the Perth Group's outlandish claims of years gone by may be coming closer to current thinking as HIV's effect on antioxidants becomes more clear. But it seems to me that the proposition that oxidative stress somehow causes the molecular effects attributed to HIV was entire illogical and unsupported. Rather it is that HIV causes the molecular effects attributed to oxidative stress...
The final set of questions, even if all were answered with a resounding yes, do NOT provide support for one theory or the other. This is a leap of logic that cannot be made, and the fact that the Perth Group persist in making them lowers their credibility. As a scientist, even if all those last 5 points were true the best one could say is that:
"It is a 50/50 chance that cellular redox change causes AIDS or that HIV causes cellular redox change."
However, with the rest of the evidence (most tellingly that HIV serostatus and replication rate best predicts the immune system damage) that practically obliterates the likelihood that cellular redox change causes AIDS.
Some good evidence for the Perth Group's argument would be measurements of SH levels and CD4 T cell counts in HIV negative members of a cohort followed for HIV seroconversion. If the oxidative stress due to the environment were to blame then SH and CD4 T cell changes should be independant of and precede HIV serostatus change.
I look forward to hearing about such longitudinal studies, which would directly contradict those of (for example) Goedert et al Science 1986: 231(4741):992-5 and Margolick et al JAIDS 1993 6(2): 153-61. Seroconversion clearly precedes disease and CD4 T cell decline, in direct contradiction of the oxidiative stress model and in clear support of the HIV/AIDS model.
If the Perth Group persist in their dogma that HIV is harmless then it does them a great diservice. Their paradigm is wrong, and it seems more sensible for them to reject it than to continue to adapt the facts to fit it.
Nick Bennett email@example.com
Competing interests: None declared