Innate immune control of influenza virus interspecies adaptation via IFITM3

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 inte...

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Main Authors: 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, Jacob S. Yount
Format: Article
Language:English
Published: Nature Portfolio 2024-10-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-024-53792-3
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author 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
Jacob S. Yount
author_facet 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
Jacob S. Yount
author_sort Parker J. Denz
collection DOAJ
description 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.
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spelling doaj-art-8acccb6fc2d840fe97cb64b953889aa72024-12-15T12:10:00ZengNature PortfolioNature Communications2041-17232024-10-0115111110.1038/s41467-024-53792-3Innate immune control of influenza virus interspecies adaptation via IFITM3Parker J. Denz0Samuel Speaks1Adam D. Kenney2Adrian C. Eddy3Jonathan L. Papa4Jack Roettger5Sydney C. Scace6Adam Rubrum7Emily A. Hemann8Adriana Forero9Richard J. Webby10Andrew S. Bowman11Jacob S. Yount12Department of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Infectious Diseases, St. Jude Children’s Research HospitalDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineDepartment of Infectious Diseases, St. Jude Children’s Research HospitalViruses and Emerging Pathogens Program, Infectious Diseases Institute, The Ohio State UniversityDepartment of Microbial Infection and Immunity, The Ohio State University College of MedicineAbstract 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.https://doi.org/10.1038/s41467-024-53792-3
spellingShingle 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
Jacob S. Yount
Innate immune control of influenza virus interspecies adaptation via IFITM3
Nature Communications
title Innate immune control of influenza virus interspecies adaptation via IFITM3
title_full Innate immune control of influenza virus interspecies adaptation via IFITM3
title_fullStr Innate immune control of influenza virus interspecies adaptation via IFITM3
title_full_unstemmed Innate immune control of influenza virus interspecies adaptation via IFITM3
title_short Innate immune control of influenza virus interspecies adaptation via IFITM3
title_sort innate immune control of influenza virus interspecies adaptation via ifitm3
url https://doi.org/10.1038/s41467-024-53792-3
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