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LY6E impairs coronavirus fusion and confers immune control of viral disease.
Pfaender, Stephanie; Mar, Katrina B; Michailidis, Eleftherios; Kratzel, Annika; Boys, Ian N; V'kovski, Philip; Fan, Wenchun; Kelly, Jenna N; Hirt, Dagny; Ebert, Nadine; Stalder, Hanspeter; Kleine-Weber, Hannah; Hoffmann, Markus; Hoffmann, Hans-Heinrich; Saeed, Mohsan; Dijkman, Ronald; Steinmann, Eike; Wight-Carter, Mary; McDougal, Matthew B; Hanners, Natasha W; Pöhlmann, Stefan; Gallagher, Tom; Todt, Daniel; Zimmer, Gert; Rice, Charles M; Schoggins, John W; Thiel, Volker.
  • Pfaender S; Institute of Virology and Immunology, Bern, Switzerland.
  • Mar KB; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • Michailidis E; Department for Molecular and Medical Virology, Ruhr-Universität Bochum, Bochum, Germany.
  • Kratzel A; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
  • Boys IN; Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA.
  • V'kovski P; Institute of Virology and Immunology, Bern, Switzerland.
  • Fan W; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • Kelly JN; Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland.
  • Hirt D; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
  • Ebert N; Institute of Virology and Immunology, Bern, Switzerland.
  • Stalder H; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • Kleine-Weber H; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
  • Hoffmann M; Institute of Virology and Immunology, Bern, Switzerland.
  • Hoffmann HH; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • Saeed M; Institute of Virology and Immunology, Bern, Switzerland.
  • Dijkman R; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • Steinmann E; Institute of Virology and Immunology, Bern, Switzerland.
  • Wight-Carter M; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • McDougal MB; Institute of Virology and Immunology, Bern, Switzerland.
  • Hanners NW; Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
  • Pöhlmann S; Deutsches Primatenzentrum, Leibniz-Institut für Primatenforschung, Göttingen, Germany.
  • Gallagher T; Faculty of Biology and Psychology, Universität Göttingen, Göttingen, Germany.
  • Todt D; Deutsches Primatenzentrum, Leibniz-Institut für Primatenforschung, Göttingen, Germany.
  • Zimmer G; Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA.
  • Rice CM; Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA.
  • Schoggins JW; Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
  • Thiel V; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA, USA.
Nat Microbiol ; 5(11): 1330-1339, 2020 11.
Article in English | MEDLINE | ID: covidwho-676586
Preprint
This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
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ABSTRACT
Zoonotic coronaviruses (CoVs) are substantial threats to global health, as exemplified by the emergence of two severe acute respiratory syndrome CoVs (SARS-CoV and SARS-CoV-2) and Middle East respiratory syndrome CoV (MERS-CoV) within two decades1-3. Host immune responses to CoVs are complex and regulated in part through antiviral interferons. However, interferon-stimulated gene products that inhibit CoVs are not well characterized4. Here, we show that lymphocyte antigen 6 complex, locus E (LY6E) potently restricts infection by multiple CoVs, including SARS-CoV, SARS-CoV-2 and MERS-CoV. Mechanistic studies revealed that LY6E inhibits CoV entry into cells by interfering with spike protein-mediated membrane fusion. Importantly, mice lacking Ly6e in immune cells were highly susceptible to a murine CoV-mouse hepatitis virus. Exacerbated viral pathogenesis in Ly6e knockout mice was accompanied by loss of hepatic immune cells, higher splenic viral burden and reduction in global antiviral gene pathways. Accordingly, we found that constitutive Ly6e directly protects primary B cells from murine CoV infection. Our results show that LY6E is a critical antiviral immune effector that controls CoV infection and pathogenesis. These findings advance our understanding of immune-mediated control of CoV in vitro and in vivo-knowledge that could help inform strategies to combat infection by emerging CoVs.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Coronavirus Infections / Coronavirus / GPI-Linked Proteins / Antigens, Surface Limits: Animals Language: English Journal: Nat Microbiol Year: 2020 Document Type: Article Affiliation country: S41564-020-0769-y

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Coronavirus Infections / Coronavirus / GPI-Linked Proteins / Antigens, Surface Limits: Animals Language: English Journal: Nat Microbiol Year: 2020 Document Type: Article Affiliation country: S41564-020-0769-y