BIOLOGY OF HUMAN AIDS RETROVIRUS

这个项目的重点是研究人类免疫缺陷的能力 病毒(HIV)感染各种人类和小鼠细胞系。CD_4基因 编码HIV感染的一个重要受体的基因在 人和小鼠细胞及其对HIV感染的易感性 用灵敏的局部免疫分析(FIA)技术进行追踪。这个 结果表明，HIV在某些人细胞(HeLa)中的感染 这与不同克隆细胞中CD4的表达水平有关。但是，在 其他人类细胞系，如U87星形胶质瘤和SCL1鳞癌 尽管cd4水平很高，但感染艾滋病毒的人很少成功。 表情。进一步的研究表明，HIV可以与CD_4结合。 这些细胞，但HIV没有进行成功的融合和进入 细胞。 这些结果表明，除了CD4外，还有其他细胞分子 是HIV进入细胞所必需的。这种可能性得到了以下方面的证实 表明当通常的艾滋病毒进入时，艾滋病毒可以感染这些人类细胞 通过使用病毒DNA来转移细胞或通过 包装在包膜蛋白中的HIV基因组假型感染 使用非CD4受体进入的小鼠逆转录病毒。 用表达基因的小鼠细胞系也进行了类似的实验。 人类的CD_4。在这些小鼠细胞中，至少有两种水平的 对艾滋病毒感染的抗药性。第一个是类似于U87的条目中的块 和SCL1人类细胞，但即使通过转基因绕过了这一障碍 或病毒伪分型，小鼠细胞仍有显著降低的水平 艾滋病毒感染。目前的数据表明，艾滋病病毒表达的减少 转基因小鼠细胞可能是由于HIV启动子和 这些小鼠细胞培养中的增强子序列。

This project has focussed on studying the ability of human immunodeficiency virus (HIV) to infect various human and mouse cell lines. The CD4 gene which encodes an important receptor for HIV infection was expressed in human and mouse cells and susceptibility of these cells to HIV infection was followed using a sensitive focal immunoassay (FIA) technique. The results indicated that HIV infection in certain human cells (HeLa) was related to the level of CD4 expression in different clones. However, in other human lines such as U87 astroglioma and SCL1 squamous cell carcinoma HIV infection was only rarely successful in spite of very high CD4 expression. Further studies indicated that HIV could bind to the CD4 on these cells, but HIV did not undergo successful fusion and entry of the cells. These results suggested that other cellular molecules in addition to CD4 were required for HIV entry of cells. This possibility was confirmed by showing that HIV could infect these human cells when the usual HIV entry mechanisms were bypassed by using viral DNA to tranfect the cells or by infecting with HIV genomes pseudotyped by packaging in envelope proteins of mouse retroviruses which use receptors other than CD4 for entry. Similar experiments were also carried out using mouse cell lines expressing human CD4. In these mouse cells, there were at least two levels of resistance to HIV infection. The first was a block in entry similar to U87 and SCL1 human cells, but even when this block was bypassed by transfection or viral pseudotyping, mouse cells still had a markedly reduced level of HIV infection. Present data suggests that the reduced HIV expression in transfected mouse cells may be due to poor functioning of HIV promotor and enhancer sequences in these mouse cell cultures.