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Pinchas Cohen
University of Southern California
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0035-8366
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SARS-CoV-2 has challenged global healthcare systems in part because its clinical manifestations are heterogeneous. Variable symptoms of SARS-CoV-2 could be attributed to the virus’ ability to mildly induce an innate immune response, as prior transcriptomic data has suggested. Mitochondrial dynamics might partially mediate the effect of SARS-CoV-2 on innate immunity. Many proteins encoded by SARS-CoV have been shown to localize to mitochondria and inhibit Mitochondrial Antiviral Signaling protein (MAVS). We analyzed multiple publicly available RNASeq data in order to unravel the metabolic and mitochondrial transcriptome signature of SARS-CoV-2 in primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report here that SARS-CoV-2 does not dramatically regulate (1) mitochondrial-gene expression or (2) MAVS expression, but (3) downregulates nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex 1 assembly. We also report cell-specific and tissue-specific effects of SARS-CoV-2 on the mitochondrial-encoded and NEM transcriptome that could inform future experimental paradigm selection.
Keywords
mitochondria, SARS-CoV-2, metabolism, RNASeq
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A new preprint design is coming!
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Pinchas Cohen
University of Southern California
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0035-8366
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 22 Jun, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
SARS-CoV-2 has challenged global healthcare systems in part because its clinical manifestations are heterogeneous. Variable symptoms of SARS-CoV-2 could be attributed to the virus’ ability to mildly induce an innate immune response, as prior transcriptomic data has suggested. Mitochondrial dynamics might partially mediate the effect of SARS-CoV-2 on innate immunity. Many proteins encoded by SARS-CoV have been shown to localize to mitochondria and inhibit Mitochondrial Antiviral Signaling protein (MAVS). We analyzed multiple publicly available RNASeq data in order to unravel the metabolic and mitochondrial transcriptome signature of SARS-CoV-2 in primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report here that SARS-CoV-2 does not dramatically regulate (1) mitochondrial-gene expression or (2) MAVS expression, but (3) downregulates nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex 1 assembly. We also report cell-specific and tissue-specific effects of SARS-CoV-2 on the mitochondrial-encoded and NEM transcriptome that could inform future experimental paradigm selection.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
This is a list of supplementary files associated with this preprint. Click to download.
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