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.
BST-2 restricts IAV release and is countered by the viral M2 protein
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Siqi Hu, Lijuan Yin, Shan Mei, Jian Li, Fengwen Xu, Hong Sun, Xiaoman Liu, Shan Cen, Chen Liang, Ailing Li, Fei Guo; BST-2 restricts IAV release and is countered by the viral M2 protein. Biochem J 1 March 2017; 474 (5): 715–730. doi: https://doi.org/10.1042/BCJ20160861
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