Published in

National Academy of Sciences, Proceedings of the National Academy of Sciences, 23(116), p. 11396-11401, 2019

DOI: 10.1073/pnas.1904493116



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Protective role for the N-terminal domain of α-dystroglycan in Influenza A virus proliferation

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Significance Influenza A virus (IAV) is a major cause of respiratory infections. We show that mice lacking the N-terminal domain of α-dystroglycan (α-DGN) exhibit significantly higher viral titers in the lungs after IAV infection. In addition, we show that overexpression of α-DGN in the lungs, both prior and during IAV infection, significantly reduces viral load and that recombinant α-DGN disrupts hemagglutination mediated by the influenza virus. Collectively, we uncover a protective role for α-DGN in IAV proliferation, suggesting it may have antiviral properties and could potentially be used as a treatment for IAV infection. As α-DGN levels are altered in more (inflammatory) disease states, this insight opens new avenues of investigation into the role of α-DGN in inflammation.