Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
HUMAN IMMUNODEFICIENCY VIRUS (HIV) GENE EXPRESSION AND FUNCTION
The Human Retroviruses. Gallo RC and Jay G, eds. San Diego, Academic Press, p. 69-106, 1991.. Unique Identifier : AIDSLINE ICDB/92678722 Haseltine WA; Dana-Farber Cancer Inst., Harvard Medical Sch., Boston, MA 02115
Abstract:
The molecular biology of HIV-1 and related human and nonhuman primate retroviruses provides a basis for understanding the peculiar pathogenesis of AIDS. Beyond the immediate practical application of the study of the molecular biology of these viruses, their study has revealed new fundamental principles regarding the mechanisms by which eukaryotic organisms control gene expression. The molecular biology of HIV-1 has provided, for the first time, both the cis- and trans-acting regulatory components that govern the fate of nascent RNA molecules within the nucleus. HIV gene expression and function are reviewed under the following headings: the virus particle (capsid proteins, replicative proteins, and the envelope proteins); establishment of infection; integration; regulation of HIV replication (long terminal repeat, trans-activator [tat], an unusual genetic switch [rev], and Tat-Rev-Env fusion protein [Tnv]); negative regulation (negative regulation factor, Nef); virion infectivity factor (Vif); viral protein U (Vpu); viral protein R (Vpr); a regulatory network; a model for progressive disease; genomic variability; and related viruses. Some of the major features of AIDS may be understood in terms of the characteristics of the virus. Life-long infection is a consequence of the life cycle of retroviruses, the formation of stably integrated viral particle genetic information into host-cell DNA. The silent infection, controlled replication, and prolific replication may be understood in terms of the interactions of the positive and negative regulatory genes that control virus growth. Selective infectivity and selective cytotoxicity of HIV-1 are primarily the consequences of the properties of the envelope glycoprotein and its interactions with the surface CD4 molecule. Concealment of the virus by regulated growth, by budding to the interior surfaces of macrophages, and by concealment with a dense cloud of sugar molecules may help to explain the failure to protect chimpanzees from infection by candidate vaccines. (147 Refs)
Keywords: Cell Transformation, Viral/GENETICS Gene Expression Regulation, Viral/*PHYSIOLOGY Genes, env/GENETICS/PHYSIOLOGY Genes, gag/GENETICS/PHYSIOLOGY Genes, pol/GENETICS/PHYSIOLOGY Genes, rev/GENETICS/PHYSIOLOGY Genes, tat/GENETICS/PHYSIOLOGY Human HIV/*GENETICS/PATHOGENICITY HIV Envelope Protein gp120/GENETICS HIV Envelope Protein gp41/GENETICS HIV Infections/*GENETICS/MICROBIOLOGY HIV Long Terminal Repeat/GENETICS/PHYSIOLOGY RNA, Messenger/GENETICS Variation (Genetics)/*GENETICS Virus Replication/*GENETICS MONOGRAPH REVIEW
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
