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SARS-CoV-2 ORF3b Is a Potent Interferon Antagonist Whose Activity Is Increased by a Naturally Occurring Elongation Variant

Authors
  • Konno, Yoriyuki1
  • Kimura, Izumi1
  • Uriu, Keiya1, 2
  • Fukushi, Masaya3
  • Irie, Takashi3
  • Koyanagi, Yoshio4
  • Sauter, Daniel5
  • Gifford, Robert J.6
  • Nakagawa, So7
  • Sato, Kei1
  • 1 Division of Systems Virology, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Institute of Medical Science, the University of Tokyo, Tokyo 1088639, Japan
  • 2 Graduate School of Medicine, the University of Tokyo, Tokyo 1130033, Japan
  • 3 Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima 7398511, Japan
  • 4 Laboratory of Systems Virology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan
  • 5 Institute of Molecular Virology, Ulm University Medical Center, Ulm 89081, Germany
  • 6 MRC-University of Glasgow Centre for Virus Research, University of Glasgow, Glasgow G61 1QH, UK
  • 7 Department of Molecular Life Science, Tokai University School of Medicine, Kanagawa 2591193, Japan
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Sep 04, 2020
Volume
32
Issue
12
Pages
108185–108185
Identifiers
DOI: 10.1016/j.celrep.2020.108185
PMID: 32941788
PMCID: PMC7473339
Source
PubMed Central
Keywords
License
Unknown

Abstract

COVID-19 pathogenesis is characterized by impaired IFN responses. Konno et al. identify ORF3b proteins of SARS-CoV-2 and related animal viruses as IFN antagonists. Their anti-IFN activity depends on the C-terminal length, and a natural ORF3b variant with increased IFN-suppressive activity was isolated from two severe COVID-19 cases.

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