The great escape: viral strategies to counter BST-2/tetherin.

The great escape: viral strategies to counter BST-2/tetherin.
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DOI:
10.1371/journal.ppat.1000913
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发表时间:
2010-05-13
期刊:
影响因子:
6.7
通讯作者:
Früh K
Früh K
中科院分区:
医学1区
文献类型:
--
作者:
Douglas JL;Gustin JK;Viswanathan K;Mansouri M;Moses AV;Früh K

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干扰素诱导的BST-2蛋白具有独特的能力,可以限制HIV-1、卡波西肉瘤相关疱疹病毒(KSHV)、埃博拉病毒和其他包膜病毒的出口。观察到病毒粒子仍然附着在BST-2表达细胞的表面,导致BST-2被重新命名为“Tetherin”。然而,HIV-1 VPU、猴免疫缺陷病毒Nef和KSHV K5等病毒蛋白可以中和BST-2,从而使成熟的病毒粒子容易从感染细胞中逃逸。自从BST-2的抗病毒功能被发现以来,对宿主和病毒之间这种有趣的相互作用的几个方面的研究出现了爆炸性增长。本文综述了BST-2限制病毒出口的分子机制以及各种病毒采取的物种特异性对策的最新工作。
The interferon-induced BST-2 protein has the unique ability to restrict the egress of HIV-1, Kaposi's sarcoma–associated herpesvirus (KSHV), Ebola virus, and other enveloped viruses. The observation that virions remain attached to the surface of BST-2-expressing cells led to the renaming of BST-2 as “tetherin”. However, viral proteins such as HIV-1 Vpu, simian immunodeficiency virus Nef, and KSHV K5 counteract BST-2, thereby allowing mature virions to readily escape from infected cells. Since the anti-viral function of BST-2 was discovered, there has been an explosion of research into several aspects of this intriguing interplay between host and virus. This review focuses on recent work addressing the molecular mechanisms involved in BST-2 restriction of viral egress and the species-specific countermeasures employed by various viruses.
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