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?:abstract
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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.
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?:creator
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?:doi
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?:doi
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10.1038/s41598-020-79552-z
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?:license
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document_parses/pdf_json/7387b56dcab8d214a49fbfea94f8ef4340b2b0a6.json
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document_parses/pmc_json/PMC7794290.xml.json
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?:publication_isRelatedTo_Disease
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?:sha_id
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?:source
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?:title
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Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples
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