人类免疫缺陷病毒包膜糖蛋白诱导CD4+细胞产生干扰和抗细胞溶解作用：艾滋病病毒持续存在的机制
Envelope glycoprotein of HIV induces interference and cytolysis resistance in CD4+ cells: mechanism for persistence in AIDS.
作者信息
Stevenson M, Meier C, Mann A M, Chapman N, Wasiak A
机构信息
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68105.
出版信息
Cell. 1988 May 6;53(3):483-96. doi: 10.1016/0092-8674(88)90168-7.
Abstract
Masking of host cell receptors following retroviral infection is the basis for the phenomenon of virus interference. Amphotropic retrovirus vectors were used to express the HIV envelope glycoprotein in a human CD4+ cell line. Envelope expression is accompanied by a reduction in the level of surface CD4 receptor molecules and correlates with the presence of intracellular envelope-CD4 receptor complexes. Cells expressing the HIV envelope acquire a cytolysis-resistant phenotype such that infection with HIV leads to a non-cytopathic persistent virus infection. Furthermore, phorbol ester-mediated stimulation of viral replication in persistently infected cells results in renewed cytolytic effects which, due to the absence of CD4 in the cell population, are absolutely independent of syncytium formation. This study elucidates the mechanism by which viral persistence is initiated and maintained in the course of AIDS.
摘要
逆转录病毒感染后宿主细胞受体的掩盖是病毒干扰现象的基础。使用嗜异性逆转录病毒载体在人CD4 +细胞系中表达HIV包膜糖蛋白。包膜表达伴随着表面CD4受体分子水平的降低，并与细胞内包膜 - CD4受体复合物的存在相关。表达HIV包膜的细胞获得了抗细胞溶解的表型，使得HIV感染导致非细胞病变的持续性病毒感染。此外，佛波酯介导的对持续感染细胞中病毒复制的刺激导致新的细胞溶解作用，由于细胞群体中不存在CD4，这些作用绝对独立于合胞体形成。本研究阐明了在艾滋病病程中病毒持续性开始和维持的机制。
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