SIV is Harmless

The establishment position is that SIV does not cause AIDS in wild African monkey populations because these populations have evolved resistance to it. Because macaques are not found naturally in Africa, they are from Asia, HIV scientists claim that macaques were never exposed to SIV in the wild and therefore could not evolve resistance to it. They claim that SAIDS has been caused in captive macaque populations by sexual transmission of SIV from other primate species native to Africa and that if these SIV infected macaques were introduced into wild macaque populations in Asia it would decimate these populations.

Lets examine the credibility of this position. Firstly, look at the standard of science purporting that SIV (cloned SIVmac) causes SAIDS in macaques and that SIV from a native African primate, the African green monkey (cloned SIVagm) causes AIDS in pig-tailed macaques but not rhesus macaques.

Kestler, H. et al, "Induction of AIDS in Rhesus Monkeys by Molecularly Cloned SIV", Science, Vol. 248, p1109-1112, June 1990:

Here the animals were not observed in tandem with an identical number of monkeys given the inoculation mixture without the cloned SIV and subjected to the same caged, and undoubtedly stressful, conditions. No account was taken of the medical history of these animals; the sample size was laughably small (11 animals in total); the inoculation mixture contained toxic and mitogenic compounds (such as IL-2 and PHA) in addition to the cloned SIV and no mention is made of the dose given; only 5 of the animals were classed as getting AIDS and this in a time frame (3.5 to 11 months) alien to that of supposedly HIV induced AIDS; no account was taken of other viruses macaques can carry that have also been claimed to cause SAIDS.....

Hirsch, V.M. et al, "Induction of AIDS by Simian Immunodeficiency Virus from an African Green Monkey: Species-Specific Variation in Pathogenicity Correlates with Extent of In Vivo Replication" Journal of Virology, Vol. 69, p 955-967, Feb 1995:

Hirsch et al continue the time-honoured, unscientific tradition of HIV/AIDS research: we have insignificantly small sample sizes, no controls using pure inoculum without the cloned SIV, no medical history of the animals is given, were they all equally wild or were some tamer than others? Do they all have identical responses to stress, even those within the same species? We are not told whether the inoculum contained just the pure clone or the usual mitogenic and oxidative toxins. There is no data concerning the presence of other infections, there is no dietary information or details of their living conditions.

A grand total of 2 rhesus macaques and 2 African green monkeys (in addition to 8 pig-tailed (PT) macaques) were given the cloned SIVagm9063 and we read on page 962 that "A gradual decline in CD4 lymphocytes (but not CD8 cells) was observed for both infected rhesus macaques; however, at present (1 year postinfection) the absolute numbers of CD4 lymphocytes have remained within normal limits for this species." After this strenuous wordplay there is no data given on the state of these animals, or the African green monkeys, two years postinfection, although curiously we do have this data, and more strenuous wordplay, for PT macaques: "Two of these animals (PT232 and PT308) cleared the initial plasma antigenemia and remained clinically stable for 2 years postinoculation. However, despite their longer survival, a progressive decline in CD4 lymphocyte levels and clinical progression have also been seen" Meaningless, half-assed studies like this would be laughed out of any real branch of science but they are very much at home in the self-validating world of HIV/AIDS.

Secondly, consider the establishment claim that natural, sexually transmitted infection in captivity is responsible for the origin of SIV in macaques (SIVmac). Why has further natural infection not ravaged these captive populations? SIVmac was first "characterised" in 1985 in two consecutive papers by Daniel et al in Science Vol. 228 spanning pages 1199 to 1204. To quote from page 1201 "An immune deficiency syndrome of macaque monkeys with many similarities to human AIDS has been described (three references given from 1983 and three from 1984); affected animals at the New England Regional Primate Centre (NERPRC) die with opportunistic infections, impaired T-cell function and lymphoproliferative disorders (reference given from 1984)." A 1986 survey showed only 3 macaques out of 848 at NERPRC had antibodies to SIV. There were similarly few cases at ERPRC and CRPRC. Only a very small proportion of macaques in captivity test positive for SIV.

Back in 1985, HIV was called HTLV-III. According to Daniel et al HTLV-I related viruses (same family as HIV) were prevalent in wild primates in both Asia and Africa. The first ever report of an HTLV-I related virus in primates came not from Africa but from Japanese macaques in the wild. Later reports also indicated the presence of HTLV-I related retroviruses in wild populations of African monkeys. How is it possible that in the wild, species of monkey separated by such wide geography can have such similar SIV related viral infections? To quote again from Daniel et al "We recently reported an association between exposure to an HTLV-I related virus and the development of spontaneous lymphoma and lymphoproliferative disorders in three species of Macaques". Were all the HTLV-I related primate viruses suddenly forgotten about or were they renamed as SIVs? What would happen if, in the wild, a "resistant" macaque with a HTLV-I related virus infected another macaque species that was na´ve for this type of virus?

Finally, the notion that African primates evolved resistance to SIV is absurd. If SIV has been around in Africa for so long that the wild primate populations have been able to evolve resistance to it then there should be almost 100% seroprevalence in all of these resistant adult populations unless the sexual transmission of SIV is inefficient. Remember these animals do not know about safe sex. Current data suggest that seroprevalence is about 50% for the "resistant" wild population with the highest seroprevalence (African Green Monkeys) and for other "resistant" wild populations it is much lower than this. The sexual transmission of SIV in the wild must therefore be very inefficient. If it is that poorly transmitted then these populations could not have evolved resistance anyway.

Consider what would happen if the probability of SIV sexual transmission is low. If the very small number of naturally resistant primates in an SIV na´ve population happened to become infected, which is very unlikely, and pass on the virus they would only be passing it on to non-resistant primates who would probably die before they could pass it to others. Bear in mind also that SAIDS occurs in a much shorter time than AIDS according to the establishment. Of the small number initially infected, most would die before they could pass the virus on. The resistant population would never dominate if SIV was so poorly transmitted.

The wild primate populations therefore cannot possibly have evolved resistance to SIV and the establishment admits that SIV does not cause SAIDS in these populations. SIV is harmless. There is no scientific foundation for the suggestion that introducing SIVmac infected macaques into SIV na´ve wild macaque populations would cause SAIDS in these populations.