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

• Published in: Cell reports (Cambridge) Vol. 32; no. 12; p. 108185
• Main Authors: Konno, Yoriyuki, Kimura, Izumi, Uriu, Keiya, Fukushi, Masaya, Irie, Takashi, Koyanagi, Yoshio, Sauter, Daniel, Gifford, Robert J., Nakagawa, So, Sato, Kei
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 22.09.2020; The Authors; Elsevier
• Subjects: Adult; Amino Acid Sequence - genetics; Animals; Betacoronavirus - genetics; Betacoronavirus - immunology; Chiroptera - virology; Codon, Nonsense - genetics; Coronavirus Infections - pathology; Coronavirus Infections - virology; COVID-19; Eutheria - virology; evolution; Humans; Interferon Type I - antagonists & inhibitors; Male; ORF3b; Pandemics; Pneumonia, Viral - virology; SARS-CoV-2; type I interferon; Viral Regulatory and Accessory Proteins - genetics; Viral Regulatory and Accessory Proteins - metabolism; COVID-19; type I interferon; SARS-CoV-2; evolution; ORF3b

One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of type I interferon more efficiently than its SARS...