tetano
Editor, Senior Moderator
Biochem J. 2017 Jan 13. pii: BCJ20160861. doi: 10.1042/BCJ20160861. [Epub ahead of print]
[h=1]BST-2 restricts IAV release and is countered by the viral M2 protein.[/h] Hu S[SUP]1[/SUP], Yin L[SUP]1[/SUP], Mei S[SUP]1[/SUP], Li J[SUP]1[/SUP], Xu F[SUP]1[/SUP], Sun H[SUP]1[/SUP], Liu X[SUP]1[/SUP], Cen S[SUP]2[/SUP], Liang C[SUP]3[/SUP], Li A[SUP]4[/SUP], Guo F[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] BST-2 (tetherin, CD317, 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 this study, we report that BST-2 diminishes the production of IAV virus-like particles, that are generated by viral NA and HA proteins, to a much greater degree than inhibits the production of wild type IAV particles. This relatively weaker inhibition of IAV is associated with reduction of BST-2 levels, which is caused by the M2 protein that interacts with BST-2 and leads to downregulation of cell surface BST-2 via the proteasomal pathway. Similar to the viral antagonist Vpu, M2 also rescues the production of HIV-1 virus-like particles and IAV virus-like particles 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.
?2017 The Author(s).
[h=4]KEYWORDS:[/h] BST-2; Host restriction factors; Influenza Virus; Innate Immunity; M2
PMID: 28087685 DOI: 10.1042/BCJ20160861
[PubMed - as supplied by publisher]
[h=1]BST-2 restricts IAV release and is countered by the viral M2 protein.[/h] Hu S[SUP]1[/SUP], Yin L[SUP]1[/SUP], Mei S[SUP]1[/SUP], Li J[SUP]1[/SUP], Xu F[SUP]1[/SUP], Sun H[SUP]1[/SUP], Liu X[SUP]1[/SUP], Cen S[SUP]2[/SUP], Liang C[SUP]3[/SUP], Li A[SUP]4[/SUP], Guo F[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] BST-2 (tetherin, CD317, 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 this study, we report that BST-2 diminishes the production of IAV virus-like particles, that are generated by viral NA and HA proteins, to a much greater degree than inhibits the production of wild type IAV particles. This relatively weaker inhibition of IAV is associated with reduction of BST-2 levels, which is caused by the M2 protein that interacts with BST-2 and leads to downregulation of cell surface BST-2 via the proteasomal pathway. Similar to the viral antagonist Vpu, M2 also rescues the production of HIV-1 virus-like particles and IAV virus-like particles 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.
?2017 The Author(s).
[h=4]KEYWORDS:[/h] BST-2; Host restriction factors; Influenza Virus; Innate Immunity; M2
PMID: 28087685 DOI: 10.1042/BCJ20160861
[PubMed - as supplied by publisher]