Garg H, Blumenthal R
Membrane Structure and Function Section, Center for Cancer Research, Nanobiology Program, National Cancer Institute, National Institutes of Health, Frederick, MD 21702-1201, USA.
Cell Mol Life Sci. 2008 Oct;65(20):3134-44. doi: 10.1007/s00018-008-8147-6.
Mechanisms of HIV-mediated CD4+ T cell loss leading to immunodeficiency are amongst the most extensively studied yet unanswered questions in HIV biology. The level of CD4+ T cell depletion in HIV infected patients far exceeds the number of infected T cells, suggesting an indirect mechanism of HIV pathogenesis termed bystander cell death. Evidence is accumulating that the HIV envelope glycoprotein (Env) is a major determinant of HIV pathogenesis and plays a critical role in bystander cell death. The complex structure and function of HIV Env makes the determination of the mechanism of Env mediated apoptosis more complex than previously thought. This review will examine the complex relationship between HIV Env phenotype, coreceptor expression and immune activation in determining HIV pathogenesis. We review data here corresponding to the role of HIV Env hemifusion activity in HIV pathogenesis and how it interplays with other AIDS associated factors such as chemokine receptor expression and immune activation.
导致免疫缺陷的HIV介导的CD4+ T细胞损失机制是HIV生物学中研究最为广泛但仍未得到解答的问题之一。HIV感染患者中CD4+ T细胞耗竭的程度远远超过被感染T细胞的数量,这表明存在一种被称为旁观者细胞死亡的HIV发病间接机制。越来越多的证据表明,HIV包膜糖蛋白(Env)是HIV发病机制的主要决定因素,并且在旁观者细胞死亡中起关键作用。HIV Env复杂的结构和功能使得确定Env介导的细胞凋亡机制比之前认为的更为复杂。本综述将探讨HIV Env表型、共受体表达和免疫激活在确定HIV发病机制中的复杂关系。我们在此回顾与HIV Env半融合活性在HIV发病机制中的作用相关的数据,以及它如何与其他艾滋病相关因素(如趋化因子受体表达和免疫激活)相互作用。