人类免疫缺陷病毒感染的分子发病机制

Arnold B. Rabson , Scott Koenig , Daryl F. Daugherty , Howard E. Gendelman
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引用次数: 4

摘要

随着人类免疫缺陷病毒(HIV)基因组的分子克隆和核苷酸序列分析,对HIV感染发病机制的分子研究进展迅速。HIV感染细胞的生化和功能研究与HIV核苷酸序列的相关性使得许多HIV蛋白的鉴定和初步功能表征成为可能。这些包括结构蛋白(gag),病毒酶(pol)和病毒调节蛋白(tat, art)。利用克隆的HIV DNA片段作为探针进行原位核酸杂交,研究HIV感染细胞在获得性免疫缺陷综合征(AIDS)和AIDS相关复合体(AIDS -related complex, ARC)患者体内的分布。这些研究表明,巨噬细胞感染是hiv诱导的神经系统疾病的重要组成部分。在被感染个体的外周血中只能发现极少量的hiv感染淋巴细胞。因此,CD4细胞耗竭在艾滋病发病机制中的作用机制尚不清楚。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular pathogenesis of human immunodeficiency virus infection

Molecular studies of the pathogenesis of human immunodeficiency virus (HIV) infections have proceded rapidly following the molecular cloning and nucleotide sequence analysis of the HIV genome. Correlation of biochemical and functional studies of HIV-infected cells with the HIV nucleotide sequence has allowed the identification and preliminary functional characterization of many HIV proteins. These include structural proteins (gag), viral enzymes (pol), and viral regulatory proteins (tat, art). Cloned HIV DNA segments have been utilized as probes for in situ nucleic acid hybridization to study the distribution of HIV-infected cells in acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) patients. These studies have demonstrated the infection of macrophages as an important component of HIV-induced neurologic disease. Only very low numbers of HIV-infected lymphocytes can be identified in the peripheral blood of infected individuals. Thus, the mechanism of CD4 cell depletion in the pathogenesis of AIDS remain obscure.

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