STRUCTURE AND FUNCTION OF HUMAN PATHOGENIC RETROVIRUSES

Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.

STRUCTURE AND FUNCTION OF HUMAN PATHOGENIC RETROVIRUSES

Retrovirus Biology and Human Disease. Gallo RC and Wong-Staal F, eds. New York, Marcel Dekker, p. 241-84, 1990.. Unique Identifier : AIDSLINE ICDB/91676226
Haseltine WA; Terwilliger EF; Rosen CA; Sodroski JG; Dana-Farber Cancer Inst., Harvard Medical Sch., Boston, MA

Abstract: Four different types of human retroviruses have been isolated: human T-cell leukemia virus type 1 (HTLV-I), the etiologic agent of the malignant adult T-cell leukemia/lymphoma; HTLV-II, a virus associated with a more benign form of T-cell leukemia/lymphoma; HTLV-II, a virus associated with a more benign form of T-cell leukemia, HIV-1 (previously called HTLV-III or LAV-1), the etiologic agent of AIDS and related disorders; and HIV-2 (also called LAV-2), a virus recently isolated from people living in West Africa. Pathogenesis and structure of these viruses are reviewed: (1) human leukemia retroviruses (pathogenesis, genomic organization [transactivation, tax protein, pp27 and pp21 proteins, mechanism of transformation, and induction of interleukin-2 receptor by the transactivator gene], and a model for HTLV-I replication and tumorigenesis) and (2) HIV (pathogenesis [HIV-2 and related simian viruses, genetics of HIV, and the long terminal repeat], structural genes [gag, pol, and env], fusion reaction mutants [CD4 binding region, fusion, gpl20-gp41 cleavage, gp120-gp41 association, and association of gp120-gp41 to the membrane], the tail of gp41, antibody recognition, regulatory genes and other proteins [vif, vpr, net, tat, rev, vpu], and a model for HIV replication and pathogenesis). It is likely that HIV-1 can establish three different states of infection: latent, controlled replication, and active proliferation. The controlled replication and selected cytotoxicity of HIV-1 account for much of the clinical spectrum of associated disease. The long asymptomatic period and accompanying low level of persistent viremia can be accounted for by controlled replication of HIV-1 in monocytes, macrophages, and T cells. The specific ablation of CD4+ cells can be attributed to attrition of the total population as a result of direct infection and subsequent cytotoxic activity of activated T cells or via syncytia formation. Any cell that expresses the envelope glycoprotein on the surface, whether the cell is killed or not, should be able to form syncytia with CD4+ cells. Syncytia, 100-500 cells large, have been observed in culture, and large syncytia have been observed in the thymus, spleen, and brain of HIV-infected patients. The failure of the immune response to prevent the continued depredations of HIV infection can be attributed, at least in part, to the failure of antibodies produced to HIV to block functional components of HIV envelope glycoprotein, including the binding and fusion reactions. (197 Refs)

Keywords: Cell Transformation, Neoplastic/GENETICS Cell Transformation, Viral/*GENETICS Cytopathogenic Effect, Viral/GENETICS Gene Expression Regulation, Viral/PHYSIOLOGY Genes, Viral/GENETICS Human HIV Infections/*MICROBIOLOGY HIV-1/*GENETICS HIV-2/*GENETICS HTLV-I/*GENETICS HTLV-II/*GENETICS Leukemia-Lymphoma, T-Cell, Acute, HTLV-I-Associated/*MICROBIOLOGY Leukemia, T-Cell, HTLV-II-Associated/*MICROBIOLOGY Receptors, Interleukin-2/GENETICS Trans-Activation (Genetics)/PHYSIOLOGY Virus Replication/GENETICS MONOGRAPH REVIEW

911130
M91B0827

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1991. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1991. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .