COFACTOR REQUIREMENT FOR CD4-MEDIATED HIV-1 ENTRY

研究。HIV-I受体CD4在许多非人类和SEE上的表达 人类细胞系不足以允许HIV-I感染。这个 研究人员描述了残留的人胶质母细胞瘤细胞系(U373) 对HIV-1的抵抗力，尽管增加了可信的CD4的表达 分子。这些细胞对H1V-1感染的阻断是菌株-1。 独立的，似乎正在病毒式进入。CD_4异核体- 表达U373(U373-CD4)的细胞与HeLa细胞融合后允许HIV-I进入。一个 U373-CD4\HeLa杂交克隆可实现高效的HIV-I复制。这些 结果提示，HeLa细胞表达一种因子(S)，可以补充 U373-CD4细胞的病毒侵入缺陷及其高效 艾滋病毒-L感染。测试额外人体细胞能力的实验 补充U373-CD4细胞的系列将提供对复杂性的洞察 病毒进入的过程。识别编码该基因的染色体的研究 互补基因和基因本身将有助于定义细胞 对CD_4介导的HIV-L感染的要求，并可能提供新的靶点 因为打断了病毒的生命周期。

Research. Expression of the HIV-I receptor CD4 on many non-human and see human cell lines is not sufficient to permit HIV-I infection. The investigator describes human glioblastoma cell line (U373) which remains resistant to HIV-1 despite the added expression of an authentic CD4 molecule. The block to H1V- 1 infection of these cells is strain- independent and appears to be at viral entry. Heterokaryons of CD4- expressing U373 (U373-CD4) cells fused to HeLa cells allow HIV-I entry. A U373-CD4\HeLa hybrid clone allows efficient HIV-I replication. These results suggest that HeLa cells express a factor(s) that can complement the viral entry defect of U373-CD4 cells and which is necessary for efficient HIV-l infection. Experiments that test the ability of additional human cell lines to complement U373-CD4 cells will provide insight into the complexity of the viral entry process. Studies to identify the chromosome encoding the complementing gene and the gene itself will help define the cellular requirements for CD4-mediated HIV-l infection and may provide new targets for interrupting the viral life cycle.