Journal article

IFITM3 and type I interferons are important for the control of influenza A virus replication in murine macrophages

Sarah L Londrigan, Linda M Wakim, Jeffrey Smith, Anne J Haverkate, Andrew G Brooks, Patrick C Reading



Abortive infection of macrophages serves as a "dead end" for most seasonal influenza A virus (IAV) strains, and it is likely to contribute to effective host defence. Interferon (IFN)-induced transmembrane protein 3 (IFITM3) restricts the early stages of IAV replication in epithelial cells, but IFITM3 restriction of IAV replication in macrophages has not been previously investigated. Herein, macrophages isolated from IFITM3-deficient mice were more susceptible to initial IAV infection, but late-stage viral replication was still controlled through abortive infection. Strikingly, IFNα/β receptor (IFNAR)-deficient macrophages infected with IAV were not only more susceptible to initial infection,..

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

Funding Acknowledgements

This study was supported by project grants APP1143154 and APP1083307 from the National Health and Medical Research Council (NHMRC) of Australia. P.C.R., S.L.L. and A.G.B are all recipients of funding from the NHMRC. The Melbourne WHO Collaborating Centre for Reference and Research on Influenza is supported by the Australian Government Department of Health.