Benefits from blocking opportunistic infections, not HIV

Protease inhibitors labeled "anti-HIV" directly block the opportunistic infections that make-up the "AIDS" definition. This fact has emerged quietly, without press attention, several years after the popular and scientific media in 1997 uncritically trumpeted corporate proclamations that these "HAART" drugs specifically targeted HIV while producing benefits, and thus confirmed the official HIV-causes--AIDS model. Two recent studies now flatly falsify any claims of HIV specificity, and offer a sensible explanation for beneficial effects that have nothing to do with HIV. This means that any evidence of HAART benefits cannot automatically bolster the HIV model, even among scientists who believe that HIV causes AIDS and that HIV tests indicate HIV infections. by Paul Philpott

Protease inhibitors directly block P. carinii and Candida

Does the popular protease inhibitor (PI) combination therapy benefit people who test HIV-positive? And, if so, how does it work?

Mainstream scientists - those who view AIDS as a distinct condition caused by HIV infection - say patients benefit dramatically from this "cocktail" therapy, also known as HAART (Highly Active Anti-Retroviral Therapy). American AIDS mortality has declined since HAART's introduction, they point out [see 'AIDS Deaths Drop'], and many patients report getting better - rising from the dead like Lazarus, the press accounts say - while on it.

Coupling these points with studies that correlate HAART with reduced HIV "viral load" and their assumption that HIV inhibition represents the HAART PI's sole capacity, these scientists believe they have confirmation for their HIV model of AIDS: HAART helps people who test HIV-positive, HIV tests indicate HIV infections, HIV infections cause AIDS, and HAART blocks HIV replication; there-fore, HIV causes AIDS.

The dissident scientists - who blame AIDS on non-HIV factors and dismiss HIV as a dud - refute this conclusion, and all of the assumptions and claims that lead up to it.

They recognize that American AIDS incidence and mortality figures both began their declines before HAART's introduction. They realize that despite all the Lazarus testimonies, so many patients become worse that no scientific study has demonstrated a clinical benefit (increased life span or improved symptoms) for HAART. As for the labeling of Pls as "HIV-specific," a growing list of serious "side effects" disproves that. The dissidents point out that the HIV scientists - the only ones who receive funds to research these issues - have failed to consider a wide scope of data that simultaneously refute the HIV-AIDS model while implicating non-HIV factors.

The dissidents conclude that these data exonerate HIV of any AIDS-causing capacity, and demonstrate that the HIV tests neither indicate nor measure active HIV infections. They substantiate these conclusions regularly in the pages of RA and in such books as Peter Duesberg's Inventing the AIDS Virus, both of which rely on references to scientific journals.

Though this dissident view explains more of the facts than the HIV model, its advocates have thus far failed to effectively address the persistent claims by some HIV-positive people that HAART relieved their AIDS conditions. If HIV tests don't indicate HIV infections, and HIV infections don't cause AIDS, then how can HAART - designed as it was to block "HIV replication"- relieve the AIDS symptoms of some people who test HIV-positive?

Until now, the dissidents had little data to convincingly answer this question.

Two relatively new scientific reports, published in the Journal of Infectious Diseases, demonstrate that the protease inhibitor drugs used in HAART strongly and directly inhibit two of the most prevalent opportunistic microbes that define AIDS: Pneumocystis carinii and Candida. Aside from representing additional evidence against the "HIV-specific" assumption for HAART PIs, these studies offer a plausible, non-HIV reason for why these drugs might indeed benefit some patients: by blocking not innocuous HIV replication, but by blocking the pathogenic replication of true disease-causing microbes.

"In Vitro Activity of HIV Pls Against Pneumocystis carinii" (Atzori, 181:1629-1634) appeared in the May 2000 issue of JID, while "In Vitro and In Vivo Anticandidal Activity of HIV Protease Inhibitors" (Cassone, 180: 448-53) ran in the August 1999 issue. Interestingly, the authors of both studies live in Italy, far away from the billions of annual USA tax dollars devoted to the HIV model of AIDS. Neither study cited any sponsor, such as drug companies, US universities, or agencies with links to that money. Nor did the reports receive any of the celebrity-like media hoopla heralding the many corporate-funded studies claiming to demonstrate HIV-based benefits for HAART

Both reports clearly proclaimed direct and significant inhibitory effects of these drugs on two of the main opportunistic infections comprised by the AIDS definition: Pneumocystis carinii, the microbe involved in P. carinii pneumonia (PCP), and Candida, the fungus involved in thrush. According to the HIV model of AIDS, these non--HIV infections erupt because HIV replication has weakened the host immune system. According to the dissident view, these opportunistic infections erupt because non-HIV factors - such as narcotics consumption or even HIV medications among affluent Westerners, or poverty among poor Africans - have weakened the host's immune system.

When HAART coincides with suppression of such symptoms as PCP or thrush, HIV scientists have always confidently attributed the favorable result to HAART's presumed inhibition of HIV. These JID papers represent the first time that funded scientists have formally considered alternative explanations.

But even these authors make sure to declare unsubstantiated allegiance to the presumptions that HAART generally benefits people who test HIV-positive, and that the benefits derive at least in part from anti-HIV effects. According to the PCP article: "Since the introduction of HIV Pls, dramatic declines in all Ols [Opportunistic Infections], including PCP, have been observed. This favorable out-come and the decline in PCP incidence is clearly due, in large part, to [immune] cell reconstitution induced by HAART," by which the authors mean anti-HIV effects.

According to the Candida article: "observational reports clearly indicate a beneficial effect of Pls" that "has been remarkably efficacious against HIV replication, AIDS progression, and mortality." The authors even make sure to present their own anti-Candida findings as an additional benefit to the "expected immunorestoration" by which they mean anti-HIV effects.

But the data from both papers make it possible to explain HAART benefits without involving the HIV-AIDS model at all. The PCP investigators found that each of the four Pls they examined (indinavir, ritonavir, nelfinavir, and saquinavir) directly suppress PCP as effectively as standard PCP medications. The Candida investigators concluded both of the Pls they examined (indinavir and ritonavir) exerted in vivo anti-Candida effects that were "particularly remarkable as they compared with the curative effects of fluconazole, a well-known anticandidal agent."

"No specific evidence that [an anti-HIV effect] is the only or the predominant effect of HAART on Ols has been provided," the Candida report states. So where are the data that compel these or any authors to attribute any observed drug benefits to "anti-HIV" effects?

These articles clearly support the dissidents, indirectly in their view that AIDS can be explained without HIV, and directly in their view that important non-HIV factors have been overlooked. The new data should embolden the call for expanding the list of variables and hypotheses considered by funded researchers.

From Rethinking AIDS the monthly publication of The Group for the Reappraisal of AIDS

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