Clapham Paul R, McKnight Áine
Center for AIDS Research, Program in Molecular Medicine, Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Biotech II, 373, Plantation Street, Worcester. MA 01605, USA1.
The Wohl Virion Center, Department of Immunology and Molecular Pathology, The Windeyer Institute for Medical Sciences, University College London, 46 Cleveland Street, London W1P 6DB, UK2.
J Gen Virol. 2002 Aug;83(Pt 8):1809-1829. doi: 10.1099/0022-1317-83-8-1809.
Human immunodeficiency virus (HIV) exploits cell surface receptors to attach to and gain entry into cells. The HIV envelope spike glycoprotein on the surface of virus particles binds both CD4 and a seven-transmembrane coreceptor. These interactions trigger conformational changes in the envelope spike that induce fusion of viral and cellular membranes and entry of the viral core into the cell cytoplasm. Other cell surface receptors also interact with gp120 and aid attachment of virus particles. This review describes these receptors, their roles in HIV entry and their influence on cell tropism.
人类免疫缺陷病毒（HIV）利用细胞表面受体附着并进入细胞。病毒颗粒表面的HIV包膜刺突糖蛋白与CD4和一种七次跨膜共受体结合。这些相互作用引发包膜刺突的构象变化，从而诱导病毒膜与细胞膜融合，并使病毒核心进入细胞质。其他细胞表面受体也与gp120相互作用并辅助病毒颗粒的附着。本综述描述了这些受体、它们在HIV进入过程中的作用及其对细胞嗜性的影响。
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