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mitted to any other member of that species can cause their immune system to become confused. What itdoes to members of other species is another question. In the mid-1970s a USSR research team was reported to have located an antibody in human faeces able to deal effectively with analmost unbelievable variety of disorders. It promised to be the ultimate antibody. There were two problems they faced, however. One; the anti- body was incredibly difficult to isolate and hold in suspension in culture. Two; it was body-specific - only effective as an antibody in that person, displaying no effect in any other individual. More recent AIDS research from the USA has revealed that massive accumulations of HIV have been found in the macroph- age lymph tissues where T4 and T8 immune cells pick up their instructions. Research indicates that 12%-58% of macrophages from AIDS patients are infected with HIV. Studies show that HIV- ° infected macrophage makes a substance that prevents T4 cells from proliferating. The T4 cell provides HIV with its incubator - without these cells it can't reproduce!lf HIV is infecting’ this es macrophage lymph tissue, why would it instruct it to stop =m producing what it needs to reproduce itself? . Is HIV something else again? As Duesberg points out, where A | D there are antibodies present with a disease the body is success- wren W t fully combating it. While those anti-bodies are present the disease isn’t likely to be fatal unless it is generating a high mortality rate among the cells it infects. HIV is detected via its antibodies - a fact calling into question HIV’s ‘killer’ image, which is further limited by the fact that the mortality rate of T4 cells in AIDS cases is between 10,000 to one and 100,000 to one, a very low rate, 5000 times slower than the minimal cell mortality required to cause death! j Y et way back in the early sixties, a Glaswegian research team discovered that when FELV-1 (feline leukaemia virus) that had developed in cats with leukaemia (though nol as the cause) was transmitted either sexually, orally or by some other exchange of body fluids, the recipient cats displayed immuno-suppression mau : , . characteristic of the later human AIDS condition (cited by Gallo). This is not the pathology of a ‘killer disease which destroys Before this transmission took place (and it should be noted the immune system’! that it took place accidently) FELV-1 was categorised as So what is HIV? endogenous. It was known not to be the cause of the leukaemia, Researchers induced leukaemia in cats, from which a retro- as this had come from human blood samples injected into the virus, FELV-1, appeared as a harmless ‘side-effect’ while it re- cats. It was considered to be a benign micro-organism -”a labo- mained in the parent organism. But when transmitted to similar ratory curiosity” as Gallo described it - a ‘side-effect’ of the organisms it causes havoc in their immune systems. Why the rearranged pathology of the cats. immune system? Do these retroviruses have an affinity with it? If they are part of the parent organism’s immune system, it’s likely After its accidental transmission had been discovered as the ‘Nae i ; i that in similar organisms they will tend to migrate to the immune cause of the immune suppression, confusion broke out among researchers as to what category is should now be placed in. system, ‘ . as As the cats were ‘unrelated’ - that is not of the same family - HIV does funny things. Sometimes it kills T-cells; sometimes researchers defined the condition as exogenous. Its it helps them grow. Sometimes it blows holes in them; sometimes ‘transmissiblity’supported this view. it merely confuses them, or does nothing at all. Its inconsistency is confusing, just as if it were confused! Professor Duesberg says HIV is not the cause of AIDS, and if anyone’s opinion on retroviruses is worth considering, his is. “If HIV is not the cause of AIDS, yet is almost constantly present with AIDS, then it is associated with AIDS in much the same way that antibodies are associated with disease - so intrinsically that HIV is detected via ‘anti-bodies’ to it. Wherever a disease goes, its antibody is never far away. And wherever AIDS is found HIV is never far behind! HIV may not be But when is a cat ‘unrelated’ to all cats? Some would say when it’s a dog - in other words itonly truly becomes ‘unrelated’ when it’s no longer of the same species. The apparent ‘unrelat- edness’ described by researchers reflects the ‘nuclear’ conceptof “relatedness in 1960s biology, rather than the ‘extended family’ view of relatedness science is approaching. In this ‘extended’ view, the ‘disease’ fills the criterion for an endogenous condition, ie that FELV-1 is ari immune response by the cats to ‘alien’ blood - in this case, human. What FELV-1 demonstrated back then has a profound effect the cause of AIDS - but could be a reaction to it #% on how we view human AIDS today. In FELV-1 we have an endogenous retrovirus with no apparent effects - exactly as John Sword Duesberg describes - occurring in one member of a species, that when transmitted to a member of the same species causes amuch Further Reading more dramatic effect similar to human AIDS. Scientific American December 1986, Sept. 1987 In other words, it looks like a body-specific immune compo- New Scientist, March 3rd, April 28th, May 5 1988 nentreleased as a response to ‘foreign’ blood, which when trans- Discovery, June 1988 NEXUS New Times Seven - Summer 1989 17 | S) | lo Cats with AIDS Y et way back in the early sixties, a Glaswegian research team discovered that when FELV-1 (feline leukaemia virus) that had developed in cats with leukaemia (though nol as the cause) was transmitted either sexually, orally or by some other exchange of body fluids, the recipient cats displayed immuno-suppression characteristic of the later human AIDS condition (cited by Gallo). Before this transmission took place (and it should be noted that it took place accidently) FELV-1 was categorised as endogenous. It was known not to be the cause of the leukaemia, as this had come from human blood samples injected into the cats. It was considered to be a benign micro-organism -’a labo- ratory curiosity” as Gallo described it - a ‘side-effect’ of the rearranged pathology of the cats, After its accidental transmission had been discovered as the cause of the immune suppression, confusion broke out among researchers as to what category is should now be placed in. As the cats were ‘unrelated’ - that is not of the same family - researchers defined the condition as exogenous. Its ‘transmissiblity’supported this view. But when is a cat ‘unrelated’ to all cats? Some would say when it’s a dog - in other words itonly truly becomes ‘unrelated’ when it’s no longer of the same species. The apparent ‘unrelat- edness’ described by researchers reflects the ‘nuclear’ concept of “relatedness in 1960s biology, rather than the ‘extended family’ view of relatedness science is approaching. In this ‘extended’ view, the ‘disease’ fills the criterion for an endogenous condition, ie that FELV-1 is ari immune response by the cats to ‘alien’ blood - in this case, human. What FELV-1 demonstrated back then has a profound effect on how we view human AIDS today. In FELV-1 we have an endogenous retrovirus with no apparent effects - exactly as Duesberg describes - occurring in one member of a species, that when transmitted to a member of the same species causes amuch more dramatic effect similar to human AIDS. In other words, it looks like a body-specific immune compo- nent released as a response to ‘foreign’ blood, which when trans- NEXUS New Times Seven - Summer 1989 mitted to any other member of that species can cause their immune system to become confused. What itdoes to members of other species is another question. In the mid-1970s a USSR research team was reported to have located an antibody in human faeces able to deal effectively with an almost unbelievable variety of disorders. It promised to be the ultimate antibody. There were two problems they faced, however. One; the anti- body was incredibly difficult to isolate and hold in suspension in culture. Two; it was body-specific - only effective as an antibody in that person, displaying no effect in any other individual. More recent AIDS research from the USA has revealed that massive accumulations of HIV have been found in the macroph- age lymph tissues where T4 and T8 immune cells pick up their instructions. Research indicates that 12%-58% of macrophages from AIDS patients are infected with HIV. Studies show that HIV- ° infected macrophage makes a substance that prevents T4 cells from proliferating. The T4 cell provides HIV with its incubator - without these cells it can't reproduce!lf HIV is infecting’ this macrophage lymph tissue, why would it instruct it to stop producing what it needs to reproduce itself? Is HIV something else again? As Duesberg points out, where there are antibodies present with a disease the body is success- fully combating it. While those anti-bodies are present the disease isn’t likely to be fatal unless it is generating a high mortality rate among the cells it infects. HIV is detected via its antibodies - a fact calling into question HIV’s ‘killer’ image, which is further limited by the fact that the mortality rate of T4 cells in AIDS cases is between 10,000 to one and 100,000 to one, a very low rate, 5000 times slower than the minimal cell mortality required to cause death! This is not the pathology of a ‘killer disease which destroys the immune system’! So what is HIV? Researchers induced leukaemia in cats, from which a retro- virus, FELV-1, appeared as a harmless ‘side-effect’ while it re- mained in the parent organism. But when transmitted to similar organisms it causes havoc in their immune systems. Why the immune system? Do these retroviruses have an affinity with it? If they are part of the parent organism’s immune system, it’s likely that in similar organisms they will tend to migrate to the immune cvieinnn system. HIV does funny things. Sometimes it kills T-cells; sometimes it helps them grow. Sometimes itblows holes in them; sometimes it merely confuses them, or does nothing at all. Its inconsistency is confusing, just as if it were confused! Professor Duesberg says HIV is not the cause of AIDS, and if anyone’s opinion on retroviruses is worth considering, his is. ” If HIV is not the cause of AIDS, yet is almost constantly present with AIDS, then it is associated with AIDS in much the same way that antibodies are associated with disease - so intrinsically that HIV is detected via ‘anti-bodies’ to it. Wherever a disease goes, its antibody is never far away. And wherever AIDS is found HIV is never far behind! HIV may not be the cause of AIDS - but could be a reaction to it # John Sword Further Reading Scientific American December 1986, Sept. 1987 New Scientist, March 3rd, April 28th, May 5 1988 Discovery, June 1988