BST-2 restricts IAV release and is countered by the viral M2 protein
BST-2 restricts IAV release and is countered by the viral M2 protein
复制标题
BST-2 限制 IAV 释放并被病毒 M2 蛋白对抗。
DOI：
10.1042/bcj20160861
复制
发表时间：
2017-03-01
影响因子：
4.1
通讯作者：
Guo, Fei
中科院分区：
文献类型：
--
作者：
Hu, Siqi;Yin, Lijuan;Guo, Fei
BST-2（tetherin、CD 317和HM 1.24）由干扰素诱导，并通过将包膜病毒拴系到细胞表面来限制病毒释放。BST-2对甲型流感病毒（IAV）感染的影响尚未确定。在本研究中，我们报告说，BST-2减少生产的IAV病毒样颗粒（VLP）所产生的病毒神经氨酸酶和血凝素蛋白的程度远远大于它抑制野生型IAV颗粒的生产。IAV的这种相对较弱的抑制与BST-2水平的降低有关，这是由与BST-2相互作用的M2蛋白引起的，并通过蛋白酶体途径导致细胞表面BST-2的下调。与病毒拮抗剂Vpu类似，M2也在BST-2存在下挽救人免疫缺陷病毒-1 VLP和IAV VLP的产生。BST-2对野生型和M2缺失型病毒的复制都有抑制作用，而M2缺失型IAV的复制受到的限制更大。这些数据揭示了IAV用于对抗BST-2限制的一种机制
BST-2 (tetherin, CD317, and HM1.24) is induced by interferon and restricts virus release by tethering the enveloped viruses to the cell surface. The effect of BST-2 on influenza A virus (IAV) infection has been inconclusive. In the present study, we report that BST-2 diminishes the production of IAV virus-like particles (VLPs) that are generated by viral neuraminidase and hemagglutinin proteins to a much greater degree than it inhibits the production of wild-type IAV particles. This relatively weaker inhibition of IAV is associated with reduction in BST-2 levels, which is caused by the M2 protein that interacts with BST-2 and leads to down-regulation of cell surface BST-2 via the proteasomal pathway. Similarly to the viral antagonist Vpu, M2 also rescues the production of human immunodeficiency virus-1 VLPs and IAV VLPs in the presence of BST-2. Replication of wild-type and the M2-deleted viruses were both inhibited by BST-2, with the M2-deleted IAV being more restricted. These data reveal one mechanism that IAV employs to counter restriction by BST-2