Role of the Endosomal ESCRT Machinery in HIV-1 Vpu-Induced Down-Regulation of BST2/Tetherin
Role of the Endosomal ESCRT Machinery in HIV-1 Vpu-Induced Down-Regulation of BST2/Tetherin
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DOI：
10.2174/157016212800792414
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发表时间：
2012-06-01
影响因子：
1
通讯作者：
Berlioz-Torrent, Clarisse
中科院分区：
文献类型：
--
作者：
Janvier, Katy;Roy, Nicolas;Berlioz-Torrent, Clarisse
细胞蛋白“骨髓基质抗原2”（BST 2，也称为Tetherin，CD 317，HM 1.24）被鉴定为针对包膜病毒传播的先天免疫防御的主要介质。BST 2显示出在感染细胞的表面物理捕获从头形成的病毒颗粒，从而减少病毒释放。慢病毒已经进化出特异性策略来下调BST 2从细胞表面的表达水平，并因此促进病毒排出。在人类免疫缺陷病毒-1（HIV-1）中，辅助蛋白Vpu对抗BST 2的抗病毒活性。然而，所涉及的细胞和分子机制尚未完全了解。Vpu介导的BST 2抗病毒活性的拮抗作用似乎涉及病毒蛋白与调节蛋白质周转和囊泡运输的宿主组分之间的复杂相互作用。本文综述了Vpu和泛素/内体途径在HIV-1对BST 2限制的对策中的相互作用，特别强调了“运输所需的内体分选复合物”（ESCRT）机制。
The cellular protein "Bone marrow stromal antigen 2" (BST2 also called Tetherin, CD317, HM1.24) was identified as a major mediator of the innate immune defense against the dissemination of enveloped viruses. BST2 was shown to physically trap the de novo formed viral particles at the surface of infected cells, thereby reducing viral release. Lentiviruses have evolved specific strategies to down-regulate the expression level of BST2 from the surface of the cells and as such promote viral egress. In Human Immunodeficiency Virus-1 (HIV-1), the accessory protein Vpu counters BST2 antiviral activity. However, the cellular and molecular mechanisms involved are not fully understood. Vpu-mediated antagonism of BST2 antiviral activity seems to involve complex interplay between the viral protein and host components regulating protein turnover and vesicular trafficking. This review focuses on the interplay between Vpu and the ubiquitin/endosomal pathway in countermeasures of HIV-1 to BST2 restriction, with a particular emphasis on the "Endosomal Sorting Complexes Required for Transport" (ESCRT) machinery.