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

Tytuł:: Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples.
Autorzy:: Miller B; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Silverstein A; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Flores M; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Cao K; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Kumagai H; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.; Graduate School of Health and Sports Science, Juntendo University, Chiba, Japan.
Mehta HH; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Yen K; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Kim SJ; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Cohen P; Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA. .
Źródło:: Scientific reports [Sci Rep] 2021 Jan 08; Vol. 11 (1), pp. 3. Date of Electronic Publication: 2021 Jan 08.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: London : Nature Publishing Group, copyright 2011-
MeSH Terms:: SARS-CoV-2*
Transcriptome*
COVID-19/*virology
DNA, Mitochondrial/*genetics
Mitochondria/*genetics
Cell Line ; Humans ; Mitochondria/virology
References:: Cell Syst. 2020 Jul 22;11(1):102-108.e3. (PMID: 32673562)
Protein J. 2020 Jun;39(3):198-216. (PMID: 32447571)
J Clin Immunol. 2006 Nov;26(6):546-54. (PMID: 17024565)
Cell Mol Immunol. 2020 Sep;17(9):998-1000. (PMID: 32728199)
Trends Endocrinol Metab. 2013 May;24(5):222-8. (PMID: 23402768)
Cell. 2011 Aug 19;146(4):645-58. (PMID: 21854988)
Nature. 2018 Aug;560(7717):238-242. (PMID: 30046113)
Nature. 2020 Jul;583(7816):459-468. (PMID: 32353859)
Trends Cell Biol. 2020 Apr;30(4):263-275. (PMID: 32200805)
EMBO Rep. 2020 Apr 3;21(4):e49799. (PMID: 32202065)
Diabetes Metab Res Rev. 2013 Mar;29(3):204-13. (PMID: 23255365)
Sci Signal. 2009 Aug 18;2(84):ra47. (PMID: 19690333)
Cells. 2019 Nov 11;8(11):. (PMID: 31717900)
Int J Mol Sci. 2019 Jul 11;20(14):. (PMID: 31373289)
J Immunol. 2014 Sep 15;193(6):3080-9. (PMID: 25135833)
Ann Intern Med. 2020 May 5;172(9):619-620. (PMID: 32160299)
Cell Res. 2018 Mar;28(3):265-280. (PMID: 29219147)
Cell Host Microbe. 2012 May 17;11(5):528-37. (PMID: 22607805)
Exp Cell Res. 2020 Aug 15;393(2):112056. (PMID: 32387288)
PLoS Pathog. 2017 Nov 10;13(11):e1006720. (PMID: 29125880)
Sci Signal. 2016 Nov 29;9(456):ra115. (PMID: 27899525)
Immunity. 2006 May;24(5):633-42. (PMID: 16713980)
Front Genet. 2021 Mar 16;12:599261. (PMID: 33796130)
J Clin Med. 2020 Apr 01;9(4):. (PMID: 32244779)
Aging (Albany NY). 2018 Jun 10;10(6):1239-1256. (PMID: 29886458)
J Mol Biol. 2013 Dec 13;425(24):5009-19. (PMID: 24120683)
Cell. 2020 May 28;181(5):1036-1045.e9. (PMID: 32416070)
Nucleic Acids Res. 2014 Apr;42(6):4100-12. (PMID: 24413562)
J Biol Chem. 2009 Aug 28;284(35):23852-9. (PMID: 19581297)
Grant Information:: T32 AG000037 United States AG NIA NIH HHS; R01AG061834 United States NH NIH HHS; R01 AG068405 United States AG NIA NIH HHS; P01 AG055369 United States AG NIA NIH HHS; RF1 AG061834 United States AG NIA NIH HHS; AG000037 United States AG NIA NIH HHS; R01 AG069698 United States AG NIA NIH HHS
Substance Nomenclature:: 0 (DNA, Mitochondrial)
Entry Date(s):: Date Created: 20210109 Date Completed: 20210122 Latest Revision: 20240111
Update Code:: 20240111
PubMed Central ID:: PMC7794290
DOI:: 10.1038/s41598-020-79552-z
PMID:: 33420163
: Czasopismo naukowe

Pełny tekst

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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