Abstract
Ever since the initial description of acquired immune deficiency syndrome (AIDS), it has been known that a specific depletion of CD4+ T-lymphocytes in the peripheral blood accompanies the onset of immunodeficiency (Gottlieb et al 1981). Following the discovery of HIV-1, Klatzmann et al (1984a) showed that the virus had a distinct tropism for and cytopathic effect in CD4+ cells. The evidence that CD4 antigen itself acts as a component of the cell surface receptor came from experiments in which HIV-1 binding, syncytium induction and infection were specifically blocked by pretreating cells with monoclonal antibodies to CD4 (Dalgleish et al 1984; Klatzmann et al 1984b; McDougal et al 1985). The cloning of the CD4 gene and cDNA allowed its expression in heterologous human cells, which then become susceptible to HIV-1 infection (Maddon et al 1986). More recently, other cell surface glycoproteins that are members of the immunoglobulin superfamily have been shown to act as viral receptors, namely ICAM-1 for the major group of rhinoviruses, and a hitherto unknown antigen as the polio receptor (White &.Littman 1989).
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Weiss, R.A., Clapham, P.R., McKeating, J.A. (1989). The Role of CD4 Antigen in HIV Infection. In: Melchers, F., et al. Progress in Immunology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83755-5_137
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DOI: https://doi.org/10.1007/978-3-642-83755-5_137
Publisher Name: Springer, Berlin, Heidelberg
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