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To Dr. Bennet, who said.
<<I would be entirely unconcerned about a positive HIV ELISA (without confirmatory WB) in a middle-aged unmarried, asymptomatic woman ...>>
It seems to me though, the analogous process is what has unfolded in South Africa and undoubtedly accounts for the absurd HIV positivity numbers that are often quoted. 
The prevelance rate in people age 55+ was found to be 7%, ***equally distribted among the sexes***. That itself is very telling, since it suggests a common, equally distributed cause for the positive results. The rate was likely higher than that because the study was voluntary, and anyone who already knew they were positive was unlikley to step forward for testing, because of the taboo associated with a positive test.
The prevalence rate in white sexually inactive SA children was found to be 11.3%. This would represent 96,000 infections, of which, only 570 could have been from MTCT (based on prevalence estimates for white females aged 15-49).
These data were based on a single Elisa.
These data suggest a VERY high false positive rate in SA and clearly call into question the specificity and reliabilty of the ELISA test at least in SA and likley everywhere else.
It seems to me that you have really argued the Perth Group's point -- that being the antigen tests are non-specific and are only supported when viewed in the context of the clinical picture and exposure to stimuli that cause the immune system to be in an ongoing, pro-inflammatory state.
On a more philosphical note, I often wonder if we are applying old disease causation models to a new situation; one that we think we understand based on successfully used older models, but is really a new situtation that is not properly explained by older models. In fact we are led down the wrong path altogether.
Imagine 100 years ago looking down a microscope and noticing that as an infection worsened, the number of WBCs increased. It would be easy to conclude that the WBCs were causing the infection and by getting rid of them, we would cure the infection.
When it comes to HIV, are we sure that we are not applying old models to a new situation and perhaps drawing the wrong conclusions. In vivo cytotoxicty of HIV has not been proven. "Isolation" of HIV is by surrogate markers -- true isolation of cultured HIV extremely difficult.
Perhaps HIV is just another opportunistic infection, like all the ones we associate with AIDS, and is really no more that that. Perhaps it is not the cause of the immune suppression, but a marker for it like all the other AIDS opportunistic infections. Perhaps the reason that HIV infection is still associated with those whose immune systems are under continual attack (be it from drugs [elicit or otherwise] mutiple sex partners, chronic infections etc.) is because this continual attack reprograms the immune system and in doing so, in time, makes it less capable of working properly and finally breaking down altogether.
Tell me why this may not also equally explain AIDS even in the presence of HIV.
1) "Nelson Mandela/HSRC Study of HIV/AIDS: South African National HIV Prevalence, Behavioural Risks and Mass Media. 2002."
Competing interests: None declared