Endogenous murine BST-2/tetherin is not a major restriction factor of influenza A virus infection

Sarah L Londrigan, Michelle Tate, Emma R Job, Jessica M Moffat, Linda Wakim, Christopher A Gonelli, Damian F J Purcell, Andrew G Brooks, Jose A Villadangos, Patrick C Reading, Justine Mintern

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Abstract

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.
Original languageEnglish
Article numbere0142925
Number of pages14
JournalPLoS ONE
Volume10
Issue number11
DOIs
Publication statusPublished - 2015

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