Abstract
Over 950,000 whole-genome sequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been determined for viruses isolated from around the world. These sequences are critical for understanding the spread and evolution of SARS-CoV-2. Using global phylogenomics, we show that mutations frequently occur in the C-terminal end of ORF7a. We isolate one of these mutant viruses from a patient sample and use viral challenge experiments to link this isolate (ORF7a Δ115 ) to a growth defect. ORF7a is implicated in immune modulation, and we show that the C-terminal truncation negates anti-immune activities of the protein, which results in elevated type I interferon response to the viral infection. Collectively, this work indicates that ORF7a mutations occur frequently, and that these changes affect viral mechanisms responsible for suppressing the immune response.
Keywords: IFN response; ORF7a; SARS-CoV-2.
【저자키워드】 SARS-CoV-2, ORF7a, IFN response, 【초록키워드】 SARS-CoV-2, viral infection, coronavirus, immune response, Mutation, severe acute respiratory syndrome Coronavirus, virus, immune modulation, type I interferon, activity, Spread, Protein, Patient, Evolution of SARS-CoV-2, IFN, experiment, change, Critical, mechanism, ORF7a, IFN response, mutant virus, viral challenge, growth defect, acute respiratory syndrome, acute respiratory syndrome coronavirus, acute respiratory syndrome coronavirus 2, growth, sequence, over, Whole-genome sequence, Affect, responsible, elevated, indicate, occur, implicated, C-terminal, 【제목키워드】 Immune suppression, SARS-CoV-2 genomic surveillance, limit, identify,