Virology of HIV

Abstract

HIV appears to have spread to humans from chimpanzees in the early 20 th century in Central Africa. Compared with other viruses, it has a relatively low transmission rate sexually or parentally. Nevertheless, it continues to spread and devastate populations in Africa, Asia and the Pacific, Eastern Europe and South America. Studies of the replication cycle of the virus have allowed the development of anti-viral agents targetted at virus binding, entry, integration and host DNA and assembly and proleolytic cleavage, as well as mechanisms of resistance allowing synthesis of second generation anti-virals targeted at resistant mutants. Elucidation of the human genome and subsequent genomic and proteomic studies are enabling a greater understanding of the interactions between the virus and host cell metabolism, including that used by the virus for refashioning cellular processes for its own benefit and evading both intra and extra-cellular, innate and adaptive immunities. The failure of recent first generation vaginal microbicide and second generation vaccine clinical trials have refocussed biomedical research efforts on understanding the mechanism of genital tract infection and often the mechanisms involved in disease progression and anti-viral immunity. Comparisons between new world and old world monkeys infected with monkey HIV (SIV) who do or do not progress to AIDS, respectively, have confirmed earlier suggestions that activation of T lymphocytes and other immune cells, especially in tissue, appears to contribute to immunosuppression and CD4 lymphocyte depletion. The roles of newly discovered T cell sub-types such as TH17 cells and T regulatory cells are currently being evaluated. New prognostic tests are being introduced for evaluation of viral resistance, viral load and CD4 lymphocyte counts in the resource poor setting and for R5/X4 phenotyping of HIV for anti-viral agents directed at interrupting HIV binding to CCR5.