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 F J Purcell; Andrew G Brooks; Jose A Villadangos; Patrick C Reading; Justine D Mintern

doi:10.1371/journal.pone.0142925

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

PLoS One. 2015 Nov 13;10(11):e0142925. doi: 10.1371/journal.pone.0142925. eCollection 2015.

Authors

Affiliations

¹ Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville, Victoria, 3010, Australia.
² Centre for Innate Immunity and Infectious Diseases, MIMR-PHI Institute of Medical Research, Clayton, Victoria, 3168, Australia.
³ Monash University, Clayton, Victoria, 3168, Australia.
⁴ Department of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, 30 Flemington Rd, Parkville, Victoria, 3010, Australia.
⁵ WHO Collaborating Centre for Reference and Research on Influenza, Victorian Infectious Diseases Reference Laboratory, at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, 3000, Australia.

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Antigens, CD / genetics*
Cell Line
Disease Models, Animal
Dogs
Epithelial Cells / virology*
Female
Gene Expression Regulation
Influenza A virus
Lung / virology
Macrophages / cytology
Macrophages / virology*
Male
Membrane Glycoproteins / genetics*
Mice
Mice, Inbred C57BL
Mice, Transgenic
Nasal Mucosa / virology
Orthomyxoviridae Infections / immunology*
Pulmonary Alveoli / cytology

Substances

Antigens, CD
BST2 protein, mouse
Membrane Glycoproteins

Grants and funding

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.