Journal article

Endogenous Murine BST-2/Tetherin Is Not a Major Restriction Factor of Influenza A Virus Infection

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

PLOS ONE | PUBLIC LIBRARY SCIENCE | Published : 2015

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 differ..

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Grants

Awarded by National Health and Medical Research Council of Australia


Awarded by National Health and Medical Research Council (NHMRC) of Australia


Funding Acknowledgements

This work was supported by funding from National Health and Medical Research Council of Australia Project Grant 1083307 (PR), National Health and Medical Research Council (NHMRC) of Australia Early Career Fellowship 1035733 (MT) and the Victorian State Government Operational Infrastructure Scheme (MT). The Melbourne WHO Collaborating Centre for Reference and Research on Influenza is supported by the Australian Government Department of Health.