Abstract:
Most animal retroviruses (RVs) are simple, passive genetic entities, whereas human RVs are more complex. There are two distinct lineages of human RVs: the leukemia viruses (human T-lymphotropic virus [HTLV]-1 and -2) and the immunodeficiency viruses (HIV-1 and -2). The first indication of greater complexity in some RVs came from studies of HTLV-1, in which a region between the envelope (env) gene and the 3' long terminal repeat was identified. This region in both HTLV-1 and -2 encodes at least two regulatory genes: tax and rex. The genome of the HIVs is even more complex; at least six accessory genes are present in addition to the gag, pol, and env genes common to all RVs. Although HTLV-1 and HIV-1 have similarities in virus regulation, there are fundamental differences in their mechanisms of pathogenesis. For HTLV-1-induced adult T-cell leukemia (ATL), there is no evidence of expression of viral genes in the patients' (pts') leukocytes. In contrast, clinical progression in HIV-infected pts correlates with, and may depend on, active virus replication and recruitment of new infected cells. These observations imply that antiviral agents would be of potential therapeutic value in pts with AIDS but not for pts with ATL and that agents that increase the level of viral replication can play a co-factor role in AIDS but not in ATL. Strategies to inhibit HIV replication can be designed around inhibition of three viral enzymes: reverse transcriptase, integrase, and protease. Other strategies can include interference in binding to cells by administration of soluble CD4 fragments, use of soluble CD4 as a targeting device, and use of inhibitors of the essential tat and rev genes of HIV. Data are now available showing that tat can transactivate a heterologous promoter, opening up the possibility that tat may transactivate other viral and cellular genes that may contribute to the overall pathogenesis of HIV infection, including Kaposi's sarcoma. (4 Refs)
Keywords: Acquired Immunodeficiency Syndrome/MICROBIOLOGY *Cloning, Molecular Cytopathogenic Effect, Viral/GENETICS Gene Expression Regulation, Viral/PHYSIOLOGY Human HIV-1/GENETICS HIV-2/GENETICS HTLV-I/GENETICS Receptors, HIV/GENETICS Retroviridae/*GENETICS Retroviridae Infections/*MICROBIOLOGY Trans-Activation (Genetics)/PHYSIOLOGY Virus Replication/*GENETICS JOURNAL ARTICLE REVIEW REVIEW, TUTORIAL 900530
M9051007
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