Dragic T, Picard L, Alizon M
Institut National de la Santé et de la Recherche Médicale U332, Institut Cochin de Génétique Moléculaire, Paris, France.
J Virol. 1995 Feb;69(2):1013-8. doi: 10.1128/JVI.69.2.1013-1018.1995.
Murine CD4+ cells are resistant to human immunodeficiency virus type 1 (HIV-1) entry and to fusion with cells expressing HIV-1 envelope glycoproteins (Env). The role of human-specific factors in Env/CD4-mediated fusion is shown by the ability of transient cell hybrids formed between CD4+ murine cells and human HeLa cells to fuse with Env+ cells. Fusion events were observed when other human cells, including erythrocytes, were substituted for HeLa cells in the hybrids. Experiments with erythrocyte ghosts showed that the factors allowing Env/CD4-mediated fusion are located in the plasma membrane. These factors were fully active after extensive digestion of erythrocytes with proteinase K or pronase. Nonprotein components of human plasma membranes, possibly glycolipids, could therefore be required for Env/CD4-mediated fusion and virus entry.
小鼠CD4+细胞对1型人类免疫缺陷病毒(HIV-1)的进入以及与表达HIV-1包膜糖蛋白(Env)的细胞的融合具有抗性。CD4+小鼠细胞与人HeLa细胞之间形成的瞬时细胞杂种与Env+细胞融合的能力表明了人类特异性因子在Env/CD4介导的融合中的作用。当杂种中的HeLa细胞被包括红细胞在内的其他人类细胞替代时,观察到了融合事件。用红细胞血影进行的实验表明,允许Env/CD4介导融合的因子位于质膜中。在用蛋白酶K或链霉蛋白酶对红细胞进行广泛消化后,这些因子仍具有完全活性。因此,人类质膜的非蛋白质成分,可能是糖脂,可能是Env/CD4介导的融合和病毒进入所必需的。