近期对TRIM5α逆转录病毒限制机制及其后果的见解。
Recent insights into the mechanism and consequences of TRIM5α retroviral restriction.
作者信息
Sastri Jaya, Campbell Edward M
机构信息
Department of Microbiology and Immunology, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153, USA.
出版信息
AIDS Res Hum Retroviruses. 2011 Mar;27(3):231-8. doi: 10.1089/AID.2010.0367.
Abstract
The cellular factor TRIM5α inhibits infection by numerous retroviruses in a species-specific manner. The TRIM5α protein from rhesus macaques (rhTRIM5α) restricts infection by HIV-1 while human TRIM5α (huTRIM5α) restricts infection by murine leukemia virus (MLV). In owl monkeys a related protein TRIM-Cyp restricts HIV-1 infection. Several models have been proposed for retroviral restriction by TRIM5 proteins (TRIM5α and TRIM-Cyp). These models collectively suggest that TRIM5 proteins mediate restriction by directly binding to specific determinants in the viral capsid. Through their ability to self-associate TRIM5 proteins compartmentalize the viral capsid core and mediate its abortive disassembly via a poorly understood mechanism that is sensitive to proteasome inhibitors. In this review, we discuss TRIM5-mediated restriction in detail. We also discuss how polymorphisms within human and rhesus macaque populations have been demonstrated to affect disease progression of immunodeficiency viruses in these species.
摘要
细胞因子TRIM5α以物种特异性方式抑制多种逆转录病毒的感染。恒河猴的TRIM5α蛋白（rhTRIM5α）限制HIV-1感染，而人类TRIM5α（huTRIM5α）限制鼠白血病病毒（MLV）感染。在夜猴中，一种相关蛋白TRIM-Cyp限制HIV-1感染。已提出了几种TRIM5蛋白（TRIM5α和TRIM-Cyp）介导逆转录病毒限制的模型。这些模型共同表明，TRIM5蛋白通过直接结合病毒衣壳中的特定决定簇来介导限制作用。通过其自我缔合的能力，TRIM5蛋白将病毒衣壳核心分隔开来，并通过一种对蛋白酶体抑制剂敏感但了解甚少的机制介导其流产性解体。在本综述中，我们详细讨论TRIM5介导的限制作用。我们还讨论了如何证明人类和恒河猴群体中的多态性会影响这些物种中免疫缺陷病毒的疾病进展。
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