Two major groups of immunodeficiency-associated retro viruses are presently known to infect man. These are human immunodeficiency virus type 1 (HIV-1) which is the recognized agent of AIDS in Central Africa, Europe, the United States, and most countries worldwide (Barre-Sinoussi et ai, 1983; Popovic et aL, 1984), and the more geographically restricted human immunodeficiency virus type 2 (HIV-2), which is most predominant in West Africa (Barin et ai, 1985; Clavel et al., 1987). Although a causative relationship between HIV-1, HIV-2 and clinical AIDS is well established (Fauci, 1988), the pathogenic mechanisms by which these viruses induce immunosuppression and disease remain unknown. Ten million individuals are currently infected with HIV worldwide and this number is expected to rise to 40 million by the year 2000 (Mann, 1992). Given the magnitude of the AIDS pandemic, new insights into the natural history of HIV-1 and HIV-2 infection as well as a better understanding of the events responsible for their recent epidemic spread are critically needed for a rational drug design and the development of effective vaccines.
Molecular characterization of HIV-1 and HIV-2, including cloning and sequence analysis of several full-length genomes, has revealed features that distinguish human AIDS viruses from the traditional RNA tumour viruses. First, the HIV-1 and HIV-2 genomes are relatively complex, each including at least six genes (in addition to the common gag, pol and env genes) termed vif, vpr, vpu (HIV-1 only), vpx (HIV-2 only), tat, rev and nef, which collectively regulate viral transcription, translation, latency and other properties that contribute to viral pathogenesis (Cullen, 1991).
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