Feng Y, Broder C C, Kennedy P E, Berger E A
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, MD 20892, USA.
Science. 1996 May 10;272(5263):872-7. doi: 10.1126/science.272.5263.872.
A cofactor for HIV-1 (human immunodeficiency virus-type 1) fusion and entry was identified with the use of a novel functional complementary DNA (cDNA) cloning strategy. This protein, designated "fusin," is a putative G protein-coupled receptor with seven transmembrane segments. Recombinant fusin enabled CD4-expressing nonhuman cell types to support HIV-1 Env-mediated cell fusion and HIV-1 infection. Antibodies to fusin blocked cell fusion and infection with normal CD4-positive human target cells. Fusin messenger RNA levels correlated with HIV-1 permissiveness in diverse human cell types. Fusin acted preferentially for T cell line-tropic isolates, in comparison to its activity with macrophagetropic HIV-1 isolates.
利用一种新型的功能互补DNA(cDNA)克隆策略,鉴定出了一种HIV-1(人类免疫缺陷病毒1型)融合与进入的辅助因子。这种蛋白质被命名为“融合素”,是一种推测的具有七个跨膜区段的G蛋白偶联受体。重组融合素使表达CD4的非人类细胞类型能够支持HIV-1包膜介导的细胞融合和HIV-1感染。针对融合素的抗体可阻断正常CD4阳性人类靶细胞的细胞融合和感染。融合素信使RNA水平与多种人类细胞类型中HIV-1的易感性相关。与对巨噬细胞嗜性HIV-1分离株的活性相比,融合素对T细胞系嗜性分离株的作用更为优先。