SARS-CoV-2 induces a muted innate immune response compared to other respiratory viruses. Mitochondrial dynamics might partially mediate this effect of SARS-CoV-2 on innate immunity. Polypeptides encoded by open reading frames of SARS-CoV and SARS-CoV-2 have been shown to localize to mitochondria and disrupt Mitochondrial Antiviral Signaling (MAVS) protein signaling. Therefore, we hypothesized that SARS-CoV-2 would distinctly regulate the mitochondrial transcriptome. We analyzed multiple publicly available RNASeq data derived from primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report that SARS-CoV-2 did not dramatically regulate (1) mtDNA-encoded gene expression or (2) MAVS expression, and (3) SARS-CoV-2 downregulated nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex I.
【저자키워드】 Gene Expression, Infection, 【초록키워드】 Transcriptome, SARS-CoV-2, Mitochondria, innate immune response, SARS-CoV, Innate immunity, lung, respiratory viruses, Protein, clinical samples, RNAseq, respiratory, expression, BALF, cellular, Signaling, Open reading frame, cell lines, MAVS, regulate, Other respiratory viruses, mitochondrial, open reading frames, cellular respiration, primary cells, polypeptides, polypeptide, RNAseq data, Complex I, clinical sample, shown, analyzed, induce, downregulated, disrupt, NEM, 【제목키워드】 Transcriptome, SARS-CoV-2, mitochondrial, Cell, clinical sample,