Alkhatib G, Combadiere C, Broder C C, Feng Y, Kennedy P E, Murphy P M, Berger E A
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.
Science. 1996 Jun 28;272(5270):1955-8. doi: 10.1126/science.272.5270.1955.
Human immunodeficiency virus-type 1 (HIV-1) entry requires fusion cofactors on the CD4+ target cell. Fusin, a heterotrimeric GTP-binding protein (G protein)-coupled receptor, serves as a cofactor for T cell line-tropic isolates. The chemokines RANTES, MIP-1alpha, and MIP-1beta, which suppress infection by macrophage-tropic isolates, selectively inhibited cell fusion mediated by the corresponding envelope glycoproteins (Envs). Recombinant CC CKR5, a G protein-coupled receptor for these chemokines, rendered CD4-expressing nonhuman cells fusion-competent preferentially with macrophage-tropic Envs. CC CKR5 messenger RNA was detected selectively in cell types susceptible to macrophage-tropic isolates. CC CKR5 is thus a fusion cofactor for macrophage-tropic HIV-1 strains.
人类免疫缺陷病毒1型（HIV-1）进入细胞需要CD4+靶细胞上的融合辅助因子。Fusin是一种异三聚体GTP结合蛋白（G蛋白）偶联受体，作为T细胞系嗜性分离株的辅助因子。趋化因子RANTES、MIP-1α和MIP-1β可抑制巨噬细胞嗜性分离株的感染，它们选择性地抑制了由相应包膜糖蛋白（Env）介导的细胞融合。重组CC CKR5是这些趋化因子的G蛋白偶联受体，它使表达CD4的非人类细胞优先与巨噬细胞嗜性Env具备融合能力。在易受巨噬细胞嗜性分离株感染的细胞类型中选择性地检测到了CC CKR5信使核糖核酸。因此，CC CKR5是巨噬细胞嗜性HIV-1毒株的融合辅助因子。
