Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
RECEPTORS FOR HUMAN RETROVIRUSES
The Human Retroviruses. Gallo RC and Jay G, eds. San Diego, Academic Press, p. 127-39, 1991.. Unique Identifier : AIDSLINE ICDB/92678724 Weiss RA; Inst. of Cancer Res., Royal Cancer Hosp., London SW3 6JB, UK
Abstract:
Retroviruses bind to cell surface receptors via their outer envelope glycoproteins, known as SU proteins. Following binding, membrane fusion probably is effected by a hydrophobic region of the transmembrane envelope protein. Fusion of many retroviruses takes place at neutral pH and is reflected by the capacity of the retrovirus to induce syncytial, multinucleated cells. Receptors for human retroviruses are reviewed, including detection of receptors; the human T-cell leukemia virus (HTLV ) receptor; the role of CD4 in HIV infection and pathogenesis; exploiting CD4-gp120 interactions for vaccines and therapy; HIV cell tropism for alternative receptors; and mechanism of HIV entry into cells. The molecular identity of the cell surface receptor for HTLV-I and HTLV-II is still not known. Syncytial and vesicular stomatitis virus pseudotype assays indicate that the receptor is widely expressed on human cell lines in culture and in several mammalian species including cat, rat, and hamster cell lines. The cell tropism exhibited by HTLV-I in cell transformation does not appear, therefore, to be determined chiefly at the receptor level. Relatively few peripheral blood lymphocytes are infected with and express HIV in infected subjects, so it has remained a puzzle as to HIV infection eventually inducing such a severe depletion of CD4+ cells and ensuing immune deficiency. In culture, a single HIV-producing cell may fuse up to 100 'bystander' CD4+ uninfected cells into giant syncytia, but giant cells are rarely seen in vivo. Knowledge of CD4-gp120 coupling has led to many studies aimed at blocking the interaction in order to prevent HIV infection or its subsequent spread within the body. Various approaches have been attempted for blocking this coupling. CD4 antigen is the principal, high-affinity receptor for HIV-1 on T lymphocytes. HIV-2 and various simian immunodeficiency virus isolates also recognize CD4 and their infection can be blocked by anti-CD4 antibodies. Although the binding of HIV to CD4 represents the first event in infection, steps in membrane fusion and internalization of the virus into cells are poorly understood. It appears that binding to CD4 is not sufficient to trigger internalization. There is some evidence that HIV enters cells via receptor-mediated endocytosis. (119 Refs)
Keywords: Antigens, CD4/GENETICS/IMMUNOLOGY AIDS Vaccines/IMMUNOLOGY Cell Transformation, Viral/*GENETICS/IMMUNOLOGY Gene Expression Regulation, Viral/*PHYSIOLOGY Human HIV/*GENETICS/IMMUNOLOGY HIV Envelope Protein gp120/GENETICS/IMMUNOLOGY HIV Infections/*GENETICS/IMMUNOLOGY HTLV-I/*GENETICS/IMMUNOLOGY HTLV-II/*GENETICS/IMMUNOLOGY Receptors, HIV/*GENETICS/IMMUNOLOGY Receptors, Virus/*GENETICS/IMMUNOLOGY T-Lymphocytes/IMMUNOLOGY/MICROBIOLOGY Virus Replication/*GENETICS/IMMUNOLOGY 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.
