tetano
Editor, Senior Moderator
PLoS One. 2015 Nov 13;10(11):e0142925. doi: 10.1371/journal.pone.0142925. eCollection 2015.
[h=1]Endogenous Murine BST-2/Tetherin Is Not a Major Restriction Factor of Influenza A Virus Infection.[/h] Londrigan SL[SUP]1[/SUP], Tate MD[SUP]2,[/SUP][SUP]3[/SUP], Job ER[SUP]1[/SUP], Moffat JM[SUP]1[/SUP], Wakim LM[SUP]1[/SUP], Gonelli CA[SUP]1[/SUP], Purcell DF[SUP]1[/SUP], Brooks AG[SUP]1[/SUP], Villadangos JA[SUP]1,[/SUP][SUP]4[/SUP], Reading PC[SUP]1,[/SUP][SUP]5[/SUP], Mintern JD[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] BST-2 (tetherin, CD317, HM1.24) restricts virus growth by tethering enveloped viruses to the cell surface. The role of BST-2 during influenza A virus infection (IAV) is controversial. Here, we assessed the capacity of endogenous BST-2 to restrict IAV in primary murine cells. IAV infection increased BST-2 surface expression by primary macrophages, but not alveolar epithelial cells (AEC). BST-2-deficient AEC and macrophages displayed no difference in susceptibility to IAV infection relative to wild type cells. Furthermore, BST-2 played little role in infectious IAV release from either AEC or macrophages. To examine BST-2 during IAV infection in vivo, we infected BST-2-deficient mice. No difference in weight loss or in viral loads in the lungs and/or nasal tissues were detected between BST-2-deficient and wild type animals. This study rules out a major role for endogenous BST-2 in modulating IAV in the mouse model of infection.
PMID: 26566124 [PubMed - in process] Free full text
[h=1]Endogenous Murine BST-2/Tetherin Is Not a Major Restriction Factor of Influenza A Virus Infection.[/h] Londrigan SL[SUP]1[/SUP], Tate MD[SUP]2,[/SUP][SUP]3[/SUP], Job ER[SUP]1[/SUP], Moffat JM[SUP]1[/SUP], Wakim LM[SUP]1[/SUP], Gonelli CA[SUP]1[/SUP], Purcell DF[SUP]1[/SUP], Brooks AG[SUP]1[/SUP], Villadangos JA[SUP]1,[/SUP][SUP]4[/SUP], Reading PC[SUP]1,[/SUP][SUP]5[/SUP], Mintern JD[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] BST-2 (tetherin, CD317, HM1.24) restricts virus growth by tethering enveloped viruses to the cell surface. The role of BST-2 during influenza A virus infection (IAV) is controversial. Here, we assessed the capacity of endogenous BST-2 to restrict IAV in primary murine cells. IAV infection increased BST-2 surface expression by primary macrophages, but not alveolar epithelial cells (AEC). BST-2-deficient AEC and macrophages displayed no difference in susceptibility to IAV infection relative to wild type cells. Furthermore, BST-2 played little role in infectious IAV release from either AEC or macrophages. To examine BST-2 during IAV infection in vivo, we infected BST-2-deficient mice. No difference in weight loss or in viral loads in the lungs and/or nasal tissues were detected between BST-2-deficient and wild type animals. This study rules out a major role for endogenous BST-2 in modulating IAV in the mouse model of infection.
PMID: 26566124 [PubMed - in process] Free full text