Re: Re: Re: Re: HIV in South Africa 30 June 2003
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Christopher S Tyler,
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Re: Re: Re: Re: Re: HIV in South Africa

A few points regarding Matthew Grove's recent post.

Matthew L Grove wrote:

"I should instead of taken issue with the idea that bidirectionality is "absolute and necessary" for a disease to spread through a male gay population, as multiple unidirectional transmission events could clearly account for spread. "

I believe the issue here is, that in order for this putative microbe to ALSO account for the vast number of assumed infections in places like Africa and Thailand, it has to be bidirectional. The HIV hypothesis must explain why heterosexual sex is said to be the predominant mode of transmission in Africa but not in the West. We can't simply be content with 'multiple unidirectional transmission events' as an explanation for gay male infections and then let it drop there.

It is generally believed that HIV originated in Africa and is related to SIV, the 'monkey version' of HIV. Is SIV said to spread unidirectionally? If HIV mutated from SIV, why would nature select unidirectional transmission (i.e., most optimally through gay male anal intercourse) as the mode of transmission? After all, if a microbe doesn't spread, it's dead.

Matthew L Grove wrote: "It is worth noting that in clearly acknowledged heterosexual bidirectionally transmissible STDs..., sex is between one infected and one non-infected partner (who then becomes infected), ie the disease spreads by multiple unidirectional events."

No. This again is incorrect. If sex happens between one infected and one non-infected partner, (who then becomes infected), regardless of role, the disease spreads by one bidirectional event. That is, the uninfected partner can receive it whether in the active or passive role.

If a female is infected, she can be completely passive and still transmit a bidirectional std to the active partner. An active infected male can transmit the bidirectionally transmitted std to the passive female.

Thus, the definition is bidirectional because it can go either way per sex act.

Matthew Grove goes on to say:

"...HIV seropositivity appears to be spreading too rapidly in South Africa for heterosexual transmission to credibly be the only route. I find the arguments that another vector might be involved (dirty needles etc) quite convincing, and certainly worthy of serious study. I don't feel this is inconsistent with HIV positivity being caused by a blood borne (and occasionally sexually transmitted) retrovirus, though."

Again an assumption is made here. That there is actually 'transmission' occuring. When we speak of transmission, we're actually talking about a reactive antibody test, and so any discussion of a 'route of transmission' must take into account the nature of the tool used to determine 'transmission'.

In the case of the HIV antibody tests (ELISA and Western Blot), it is known that many agents and conditions can cause them to be reactive, some of which are endemic to areas such as South Africa. For instance, antibodies directed against mycobacterium (M. leprae, M. tuberculosis, M. avium-intracellulare) significantly cross-react with the HIV antibody tests, leading researchers such as Kashala and Essex to state, "ELISA and WB may not be sufficient for HIV diagnosis in AIDS-endemic areas of Central Africa where the prevalence of mycobacterial diseases is quite high";(1)

The Perth Group highlight these (and other) problems in an article within volume 13 of Current Medical Research and Opinion: Since antibodies to mannans, including those contained in the walls of all fungi (Candida albicans, Cryptococcus neoformans, Coccidioides immitis, Histoplasma capsulatum, including Pneumocystis carinii),(2-14) react with the "HIV proteins" then, as Essex and his colleagues (1) have pointed out for mycobacterial infection in Africa, one would expect the sera of all people infected with fungi and mycobacteria to cross-react with the "HIV-1 glycoproteins" as well as to cause "significant cross- reactivities with HIV-1 pol and gag proteins". (5)

Thus, it is necessary not to make an assumption that just because an antibody test is reactive that transmission of a retrovirus has taken place. Even something as simple as malnutrition will cause reactivity in the HIV tests.

With regard to the Padian study, it may be dismissed as flawed, but at the end of the day, it mirrors the lack of a spread of HIV/AIDS in the general heterosexual population in the United States and Europe (this in-spite of the 'every one at risk' dire predictions of the 80's and 90's). After 23 years, HIV/AIDS is still primarily confined to the original risk groups.

And what do we have to show for these 23 years of the HIV hypothesis?

We have flawed, non-specific, non-standardizerd, non-reproducible antibody tests. The general public are given assurance as to their high degree accuracy, and in whose name those who are unlucky enough to be found positive (pick your criteria) are given a death sentence (prognostication).

We have drugs like the failed chemotherapy agent AZT which was approved on the basis of fraudulent human trials. A drug that has been responsible for the agonizing death of many thousands. How many people knew to even ask their doctor if AZT was converted sufficiently into its active form, AZTTP, in order to have an antiretroviral effect? How many doctors were even aware that only a small fraction of AZT is triphosphorylated by cellular enzymes and thus can't possibly have an antiretroviral effect. How many people were told by their doctors that AZT would eat away the lining of their intestines giving them horrible stomach pain, destroy their muscle tissues and kill their bone marrow? No. We're told to trust our doctors and scientists.

And we have the protease inhibitors that have mamed and disfigured many more. Facial wasting, buffalo humps, extended bellies, increased heart disease, increased diabetes, stick-like limbs, destroyed livers. In fact, end organ liver failure is now the leading cause of death among those taking them. I would encourage every scientist, doctor, or student on this board to go on the cocktail for a year and then tell us how wonderful and lifesaving these drugs are; how they're extending lives and making people live longer.

On the other hand, the Perth Group offers an hypothesis that leads the way non-toxic, inexpensive, and health-building antioxidants. I know more than one man who has been able to rebuild their bodies with the help of their oxidative stress theory after having had their bodies ruined by the cocktail.

Why is the world so opposed to what they have to offer, when the HIV hypothesis so far has offered a death sentence (antibody tests), and poisons (AZT, Navirapine, etc.)?

Chris Tyler

1. Kashala O, Marlink R, Ilunga M, et al. (1994). Infection with human immunodeficiency virus type 1 (HIV-1) and human T cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. J. Infect. Dis. 169:296-304.

2. Ezekowitz RA, Williams DJ, Koziel H, et al. (1991). Uptake of Pneumocystis carinni mediated by the macrophage mannose receptor. Nature 351:155-158.

3. Hoffman OA, Standing JE, Limper AH. (193). Pneumocystis carinni stimulates tumor necrosis factor-alpha release from alveolar macrophages through a beta-glucan-mediated mechanism. J. Immunol. 150:3932-3940.

4. O?Riordan DM, Standing JE, Limper AH. (1995). Pneumocystis carinni glycoprotein A binds macrophage mannose receptors. Infect-Immun 63:779-784.

5. Eleni Papadopulos-Eleopulos, Valendar F.Turner, John M Papadimitriou, Gordon Stewart, and David Causer. HIV ANTIBODIES: FURTHER QUESTIONS AND A PLEA FOR CLARIFICATION. Current Medical Research and Opinion. Vol. 13: 627-634, 1997

Competing interests:   None declared