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Endomembrane targeting of human OAS1 p46 augments antiviral activity.
Soveg, Frank W; Schwerk, Johannes; Gokhale, Nandan S; Cerosaletti, Karen; Smith, Julian R; Pairo-Castineira, Erola; Kell, Alison M; Forero, Adriana; Zaver, Shivam A; Esser-Nobis, Katharina; Roby, Justin A; Hsiang, Tien-Ying; Ozarkar, Snehal; Clingan, Jonathan M; McAnarney, Eileen T; Stone, Amy El; Malhotra, Uma; Speake, Cate; Perez, Joseph; Balu, Chiraag; Allenspach, Eric J; Hyde, Jennifer L; Menachery, Vineet D; Sarkar, Saumendra N; Woodward, Joshua J; Stetson, Daniel B; Baillie, John Kenneth; Buckner, Jane H; Gale, Michael; Savan, Ram.
Afiliação
  • Soveg FW; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Schwerk J; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Gokhale NS; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Cerosaletti K; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Smith JR; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Pairo-Castineira E; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Kell AM; Benaroya Research Institute at Virginia Mason, Seattle, United States.
  • Forero A; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Zaver SA; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Esser-Nobis K; Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom.
  • Roby JA; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Hsiang TY; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Ozarkar S; Department of Molecular Genetics and Microbiology, School of Medicine, University of New Mexico, Albuquerque, United States.
  • Clingan JM; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • McAnarney ET; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Stone AE; Department of Microbial Infection and Immunity, College of Medicine, The Ohio State University, Columbus, United States.
  • Malhotra U; Department of Microbiology, School of Medicine, University of Washington, Seattle, United States.
  • Speake C; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Perez J; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Balu C; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Allenspach EJ; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Hyde JL; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Menachery VD; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Sarkar SN; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Woodward JJ; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Stetson DB; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Baillie JK; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
  • Buckner JH; Department of Microbiology and Immunology, University of Texas Medical Center, Galveston, United States.
  • Gale M; Department of Immunology, School of Medicine, University of Washington, Seattle, United States.
  • Savan R; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, United States.
Elife ; 102021 08 03.
Article em En | MEDLINE | ID: mdl-34342578
Many host RNA sensors are positioned in the cytosol to detect viral RNA during infection. However, most positive-strand RNA viruses replicate within a modified organelle co-opted from intracellular membranes of the endomembrane system, which shields viral products from cellular innate immune sensors. Targeting innate RNA sensors to the endomembrane system may enhance their ability to sense RNA generated by viruses that use these compartments for replication. Here, we reveal that an isoform of oligoadenylate synthetase 1, OAS1 p46, is prenylated and targeted to the endomembrane system. Membrane localization of OAS1 p46 confers enhanced access to viral replication sites and results in increased antiviral activity against a subset of RNA viruses including flaviviruses, picornaviruses, and SARS-CoV-2. Finally, our human genetic analysis shows that the OAS1 splice-site SNP responsible for production of the OAS1 p46 isoform correlates with protection from severe COVID-19. This study highlights the importance of endomembrane targeting for the antiviral specificity of OAS1 and suggests that early control of SARS-CoV-2 replication through OAS1 p46 is an important determinant of COVID-19 severity.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: 2',5'-Oligoadenilato Sintetase / SARS-CoV-2 / COVID-19 Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: 2',5'-Oligoadenilato Sintetase / SARS-CoV-2 / COVID-19 Idioma: En Ano de publicação: 2021 Tipo de documento: Article