Abstract
Soon after the identification of HIV as the causative agent of AIDS, it became clear that CD4 was its primary cellular receptor. The clinical observation that AIDS was characterized by a loss of the T helper/inducer subset of lymphocytes (Th) prompted the studies which showed that HIV replicated in vitro only in cells expressing the Th marker, CD4 (Klatzmann et al. 1984a), and that antibodies to CD4 specifically inhibited infection and syncytium formation (Dalgleish et al. 1984; Klatzmann et al. 1984b). The receptor function of CD4 was conclusively demonstrated when its expression was shown to confer HIV susceptibility on previously insusceptible cells (Maddon et al. 1986). Finally, when recombinant soluble CD4 was mixed with virus or virus-infected cells, infection and syncytium formation were inhibited, presumably because of competition with the cell surface receptor (Smith et al. 1987; Fisher et al. 1988; Hussey et al. 1988; Traunecker et al. 1988).
Keywords
- Human Immunodeficiency Virus
- Human Immunodeficiency Virus Infection
- Envelope Glycoprotein
- Syncytium Formation
- Gp120 Binding
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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James, W., Weiss, R.A., Simon, J.H.M. (1996). The Receptor for HIV: Dissection of CD4 and Studies on Putative Accessory Factors. In: Littman, D.R. (eds) The CD4 Molecule. Current Topics in Microbiology and Immunology, vol 205. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79798-9_7
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