AIDS: Caused by development of resistance to drugs in a non-target intracellular parasite

The origin of acquired immune disorder syndrome (AIDS) has been the subject of substantial controversy both in the scientific community and in the popular press. The debate involves the mode of transmission of a simian virus (SIV) to humans. Both major camps in the argument presume that humans are normally free of such viruses and assume that once the simian virus was transmitted, it immediately infected some T-cells and caused the release of toxic agents that killed off bystander (uninfected) T-cells resulting in AIDS. The evolution of the Simian virus (SIV) into a human virus (HIV) is regarded as an artifact. In contrast, a fundamentally different hypothesis has been proposed [Parris GE. Med Hypotheses 2004;62(3):354–7] in which it is presumed that in hyper-endemic areas of malaria (central Africa), all primates (humans and non-human primates) have shared a retrovirus that augments their T-cell response to the malaria parasite. The virus can be called “primate T-cell retrovirus” (PTRV). Over thousands of years the virus has crossed species lines many times (with little effect) and typically adapts to the host quickly. In this model, AIDS is seen to be the result of the development of resistance of the virus (PTRV) to continuous exposure to pro-apoptotic (schizonticidal) aminoquinoline drugs used to prevent malaria. The hypothesis was originally proposed based on biochemical activities of the aminoquinolines (e.g., pamaquine (plasmoquine(TM)), primaquine and chloroquine), but recent publications demonstrated that some of these drugs definitely adversely affect HIV and other viruses and logically would cause them to evolve resistance. Review of the timeline that has been created for the evolution of HIV in humans is also shown to be qualitatively and quantitatively consistent with this hypothesis (and not with either version of the conventional hypothesis). SARS and Ebola also fit this pattern.