Cited by 87SARS-CoV-2 and COVID-19 Researchinterferon and immune responsesMitochondrial Function and Pathology

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

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Miller, Brendan, Silverstein, Ana, Flores, Melanie, Cao, Kevin, Kumagai, Hiroshi, Mehta, Hemal H., Yen, Kelvin, Kim, Su- Jeong +1 more·2021·Scientific Reports

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.

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  • Nuclear-encoded mitochondrial genes related to cellular respiration and Complex I are downregulated during SARS-CoV-2 infection.

    “A recent paper described the downregulation of nuclear-encoded mitochondrial genes related to cellular respiration and Complex I during infection with SARS-CoV-2, suggesting that proper mitochondrial function of immune cells is essential for containing viral propagation183.”

    From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [183]

  • Proper mitochondrial function of immune cells is essential for containing viral propagation.

    “A recent paper described the downregulation of nuclear-encoded mitochondrial genes related to cellular respiration and Complex I during infection with SARS-CoV-2, suggesting that proper mitochondrial function of immune cells is essential for containing viral propagation183.”

    From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [183]

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Authors
Miller, B., Silverstein, A., Flores, M., Cao, K., Kumagai, H., Mehta, H. H., Yen, K., Kim, S. J., & Cohen, P.
Affiliations
University of Southern California (US)
Corresponding author
Cohen, Pinchas
Venue
Scientific Reports
Published
2021-01-08
Volume
11
Issue
1
Pages
3-3
ISSN
2045-2322 (ISSN-L)
OpenAlex
W3120873513
Cited by
86
References
31
Citations by year
2026: 4 · 2025: 8 · 2024: 22 · 2023: 15 · 2022: 22 · 2021: 15
FWCI
5.94
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institute on Aging (AG000037)
  • National Institutes of Health (R01AG061834)
  • National Institutes of Health,United States (P01AG034906)
Topics
  • Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
SARS-CoV-2, mitochondrial transcriptome, mitochondrial dynamics, innate immune response, mitochondrial antiviral signaling, nuclear-encoded mitochondrial genes, cellular respiration, complex I, lung, bronchoalveolar lavage fluid
MeSH terms
COVID-19, SARS-CoV-2, Cell Line, DNA, Mitochondrial, Humans, Mitochondria, Transcriptome

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