Innate immune control of influenza virus interspecies adaptation via IFITM3

Parker J. Denz, Samuel Speaks, Adam D. Kenney, Adrian C. Eddy, Jonathan L. Papa, Jack Roettger, Sydney C. Scace, Adam Rubrum, Emily A. Hemann, Adriana Forero, Richard J. Webby, Andrew S. Bowman and Jacob S. Yount ()
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Parker J. Denz: The Ohio State University College of Medicine
Samuel Speaks: The Ohio State University College of Medicine
Adam D. Kenney: The Ohio State University College of Medicine
Adrian C. Eddy: The Ohio State University College of Medicine
Jonathan L. Papa: The Ohio State University College of Medicine
Jack Roettger: The Ohio State University College of Medicine
Sydney C. Scace: The Ohio State University College of Medicine
Adam Rubrum: St. Jude Children’s Research Hospital
Emily A. Hemann: The Ohio State University College of Medicine
Adriana Forero: The Ohio State University College of Medicine
Richard J. Webby: St. Jude Children’s Research Hospital
Andrew S. Bowman: The Ohio State University
Jacob S. Yount: The Ohio State University College of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-11

Abstract: Abstract Influenza virus pandemics are caused by viruses from animal reservoirs that adapt to efficiently infect and replicate in human hosts. Here, we investigate whether Interferon-Induced Transmembrane Protein 3 (IFITM3), a host antiviral factor with known human deficiencies, plays a role in interspecies virus infection and adaptation. We find that IFITM3-deficient mice and human cells can be infected with low doses of avian influenza viruses that fail to infect WT counterparts, identifying a new role for IFITM3 in controlling the minimum infectious virus dose threshold. Remarkably, influenza viruses passaged through Ifitm3−/− mice exhibit enhanced host adaptation, a result that is distinct from viruses passaged in mice deficient for interferon signaling, which exhibit attenuation. Our data demonstrate that IFITM3 deficiency uniquely facilitates potentially zoonotic influenza virus infections and subsequent adaptation, implicating IFITM3 deficiencies in the human population as a vulnerability for emergence of new pandemic viruses.

Date: 2024
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DOI: 10.1038/s41467-024-53792-3

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