The long-term survival of the pathogen in a vertebrate host depends on proper balance (or evasion) of the pathogen with the host's immune system. A possibly critical factor of difference among modern humans, the Stone Age man, and the modern non-human primate needs to be recognized here. Some of the possible differences would make the response greater or weaker, and could consequently support or conflict with the hypothesis proposed here. This balance could depend on the variety and extent of immune stimulation in general and is in addition to the responses of these host species to their particular retroviruses. The stimulation of the immune system, variety of stimulations, and the age dependency of individuals exposed to other antigens before they are challenged by viral antigen do vary greatly (see for example, Miedema and Klein, 1996). There must be marked differences in the antigenic stimulation of the members of primate societies in the wild, the humans in developing countries, and the humans in developed countries. Either too much, too little, or the wrong kind of stimulation may mean that the immune system, particularly the mucosal part of the system, will be either over or under active. A slight variation may eliminate the pathogen or fail to prevent new pathogens from entering and supplanting the original one. The immune system may be secondarily modified by destruction of certain specialized T-cells which respond to the HIV or SIV pathogens. As a speculative example, female chimpanzees engage in some sexual activity for some time before they become pregnant. If the female has been infected with SIV for several years before she becomes fecund, it would not be surprising if she had slowly developed a range of mucosal immune responses that would have a protective effect on her developing fetus. This effect might not occur if she had been infected just prior to becoming pregnant. Some aspects of the AIDS disease process in humans, it is well known, are similar to autoimmune diseases and the destruction of cells of the immune system bearing viral or similar receptors. All that is being suggested here is that such phenomena need be only slightly altered in the not quite yet-adapted HIV-human pair from those of naturally adapted retrovirus-primate pairs to give virulent disease. In the current world AIDS epidemic these could affect timing of symptom onset and the severity of debilitating disease.
At an earlier time when our blood supplies were contaminated, hemophiliacs were very likely to receive the AIDS virus and become HIV seropositive. A significant point is that their time to conversion to ARC and to fulminating AIDS was 90% longer than other non-hemophiliac seropositive persons at that time (Darby et al., 1995). One possible reason is that the medically treated hemophiliacs were being continuously challenged and immunized against a large variety of other substances that were present in the various blood transfusions that they regularly received. An additional factor concerning the AIDS disease in the past was that when hemophilia patients were initially infected by transfusion, the disease would have been started with a much larger number of viruses than that transmitted by usual or unusual sexual practices or by a drug addict's re-used needle. Consequently, their immune system was stimulated in a way that the immune systems of normal people infected by sexual contact are not, simply because the intensity of the immune challenge for the hemophiliac was greater. These possibilities raise the suggestion that African green monkeys are immunologically equivalent to human hemophiliacs receiving blood transfusions. As a result, an African green monkey from which SIV can be isolated might have an especially effective immune system and be able to continuously destroy a much larger proportion of retroviruses and thus limit the viremia. This could mean that it would live for a long time before it would become immunologically deficient. In any case, it will be interesting to see the disease progression in fresh hemophiliac patients that were infected by sexual transmission and not any more by transfusions now that they receive recombinant clotting factors without these multiple sources of diverse immunogenic stimulation or of HIV. This could be a test of the proposed theory.
Immune reactivity can depend on the presence of other pathogens. Infection with mycoplasma, Herpes, Epstein-Barr, and several other viruses may affect how HIV infection leads to the immune deficiency state. With co-infection of such viruses, it is likely that the time at which AIDS erupts may be sped or slowed in either the human or monkey. This raises the possibility that a different spectrum of viruses and other ubiquitous diseases of a species of a host might influence the course of a retroviral disease. A sometimes-symptomless retrovirus infection that leads to the development of a debilitating immune deficiency might do so differently when infecting a different host species. On the contrary, other pathogens may trigger the emergence of the AIDS virus from the host's chromosomes. These assorted immunological events could greatly affect the life history of a retrovirus in any new primate host. Consequently, it can be argued that the AIDS virus may well have been adapted to be "gentle" and virtually un-obstructive in an old host, but at present in humans, those strategies do not work the same because the human pathogenicity is different. Because of our social organization, our life expectancy, and our antigenic environment, the outcome of this parasitism could well be quite different. Possibly the finding is relevant to the case of an individual that became infected with only one strain even though two different varieties of HIV were transfused simultaneously into him (Diaz etal., 1996).
A very striking observation was made several years ago (see Mitler, Antia, and Levin 1996) and considers the significance of the two experimental publications. The major conclusion is that the HIV viruses grow very rapidly and are very rapidly destroyed by the apparently healthy, but HIV positive, individuals. It leaves unanswered how much of this destruction is due directly to the action of the host versus the action of the host as modified by the virus. However, there is the possibility that to some degree this is due to mechanisms implemented by the resident HIV virus.
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