In the unscientific world of HIV/AIDS things apparent are automatically taken as real. The fact that AZT is very inefficiently triphosphorylated and therefore cannot possibly have the anti-HIV effect that is claimed for it (see Current Medical Research and Opinion 1999, Vol. 15, supplement 1) would be sufficient in itself to cause any unbiased and thoughtful person to question its utility in the prevention of mother to child transmission (MTCT) of "HIV". AZT was never designed as an anti-HIV drug by the way.
Elsewhere on this site I provided a critique (reproduced below) of the study ACTG 076, the best that AIDS Inc. can do in support of the notion that AZT prevents the MTCT of "HIV". There are also some studies claiming to show that vitamin A also reduces the MTCT of "HIV"(1 to 3). Given that AZT is highly toxic (skull and crossbones on reagent label), and a rather expensive poison also, one wonders why the use of cheap, non-toxic vitamin A has not by now been implemented by the AIDS establishment as health policy across the whole of sub-saharan Africa.
With the exception of vitamin A, no studies have been conducted to evaluate the effect of antioxidants (reducing agents) upon MTCT of "HIV". In 1983 Luc montagnier and in 1984 Robert Gallo stimulated cell cultures from tissues of AIDS patients with numerous oxidising (4) and mitogenic chemical agents and observed a number of phenomena which, long before the AIDS era, were known to be non-specific. By 1986 Montagnier and Gallo acknowledged that the "HIV" phenomena cannot be detected unless the cells are stimulated (5, 6). Subsequently researchers including Anthony Fauci, showed that when stimulated cell cultures are treated with reducing agents this greatly suppresses the appearance of such phenomena (7). From the beginning of the AIDS era there has been evidence that individuals belonging to the AIDS risk groups are exposed to oxidising agents. In a 1998 study, researchers from Canada reported that supplementation of vitamin E and C reduces oxidative stress in "HIV" positives and produces a trend towards a reduction in "viral load"(8). I quote:
"This study is the first randomised controlled trial to demonstrate that, in an HIV-positive population, daily supplementation of 800 IU vitamin E and 1000 mg vitamin C significantly decreases oxidative stress and produces a trend towards a reduction in HIV viral load suggesting that there may be some clinical benefit worthy of larger clinical trials. Since combination antiretroviral therapies containing protease inhibitors are limited for economic reasons to only about 10% of HIV infected individuals in the world, consideration of the potential for this antioxidant therapy remains important for the developing world. It could have great benefit, perhaps similar to the effect of vitamin A supplementation on childhood mortality in developing countries."
Many factors involving antigenic stimulation (eg. vaccines, pathogens) can also increase "viral load" and therefore effect the presumed MTCT of "HIV" (9, 10). We have been pointing out for a long time that if HIV causes AIDS then significant "HIV replication" should precede AIDS defining disease but actually the reverse is true (10).
Sadly, no matter how many rational objections to the HIV/AIDS construct we present, we cannot hope to make any impact upon the edifice of a globally held establishment dogma founded upon fear, faith and finance. Our efforts can, however, serve to get the message out to those capable of thinking outside the mental maps imposed by the corporate driven medico-scientific establishment.
1. Semba et al (1994) Maternal Vitamin A deficiency and Mother to child Transmission of HIV-1, Lancet 343:1593-7
2. Semba et al (1997) Viamin A Deficiency and Maternal Infant Transmissions of HIV in two Metropolitan areas in the United States, AIDS 11:325-32
3. Coutsoudis et al (1999) Randomised trial testing the effect of vitamin A supplementation on pregnancy outcomes and early HIV-1 mother to child transmission in Durban, South Africa. South African Vitamin A Study Group AIDS 13:1517-24
4. Sekkat et al (1988) Oxidative phenomena are implicated in human T-cell stimulation. Immunology, 63:431-437
5. Klatzmann and Montagnier (1986) Approaches to AIDS therapy. Nature 319:10-11
6. Zagury et al (1986) Long term cultures of HTLV-III-infected T cells: A model of cytopathology of T-cell depletion in AIDS. Science, 231:850-853
7. Fauci et al (1991) Suppression of human immunodeficiency virus expression in chronically infected monocytic cells by glutathione, glutathione ester and N-acetyl cysteine. Proc. Natl. Acad. Sci. USA 88:896-990
8. Allard et al (1998) Effects of vitamin E and C supplementation on oxidative stress and viral load in HIV infected subjects. AIDS, 12:1653-9
9. O Brien et al (1995) Human immunodeficiency virus-type 1 replication can be increased in peripheral blood of seropositive patients after influenza vaccination. Blood 86:1082-9
10. Donovan et al (1996) Changes in virus load markers during AIDS-associated opportunistic diseases in human immunodeficincy virus infected persons. Journal of Infectious Diseases. 174:401-3
I asked for a scientific journal article to support the statistic you gave. I only have time to address one study. Your link
talks about the ACTG 076 study which is generally considered the definitive one so I will deal with that.
ACTG 076 is proclaimed as the ONLY "randomised double blind placebo controlled" trial of the effect of AZT on MTCT of HIV although the authors saw fit to retain as priveleged information how it was rendered double-blind and randomised. The researchers required 59 institutions in two continents to recruit 477 mothers. There are several concerns about the criteria for positivity used in this study.
As is often the case in HIV/AIDS, statistics generated by a paper are uncritically accepted with out any scrutiny of the assumptions or procedures used.
This paper purports to show an absolute reduction in HIV positivity of 17.2% but it is customary to promote the relative reduction value of 67.5% instead. Testing was done at birth, 12, 24 and 78 weeks, testing was stopped for each infant found positive.
Given the 95% confidence intervals, the study could show no estimated difference in infectivity between the AZT and placebo groups at 6 weeks. At least 92% of infected infants would have detectable virus at 14 days and certainly all of those infected by MTCT would have detectable virus by 6 weeks. By week 78 of this study 28 more infants in the placebo group were "infected" than in the AZT group on the basis of at least one HIV positive culture. It is reasonable to conclude that these 28 were not "infected" by maternal transmission. This study does not prove that AZT reduces MTCT of HIV.
AZT could provide an apparent reduction in positivity. AZT disrupts triphosphorylated nucleotide pools in cells (Proc. Natl. Acad. Sci. USA 1986, Vol. 83:8333-8337) and has a general cytostatic effect, under these conditions there will generally be fewer RNA transcripts to be picked up by the "viral load" test*. If there are fewer RNA transcripts there will also be less p24 antigen translation and therefore a lower incidence of "HIV isolation"**. AZT also has a mutagenic capacity and PCR primers are obtained from cell cultures derived from antiretroviral na´ve individuals, this may cause "HIV" nucleic acids to be less efficiently amplified in the presence of AZT.