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Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples.


ABSTRACT: 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.

SUBMITTER: Miller B 

PROVIDER: S-EPMC7794290 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples.

Miller Brendan B   Silverstein Ana A   Flores Melanie M   Cao Kevin K   Kumagai Hiroshi H   Mehta Hemal H HH   Yen Kelvin K   Kim Su- Jeong SJ   Cohen Pinchas P  

Scientific reports 20210108 1


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  ...[more]

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