Sly Saint
Senior Member (Voting Rights)
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.
https://www.nature.com/articles/s41598-020-79552-z
see also article about the research
https://www.thailandmedical.news/ne...-host-constant-fatigue-could-result-from-thisThe study findings were published in the peer reviewed journal: Scientific Reports By Nature. https://www.nature.com/articles/s41598-020-79552-z
The scientists discovered an important line of attack used by the novel coronavirus: it targets the mitochondria, which not only generate the energy that powers a cell's biochemical reactions but also play important roles in immune function.
Dr Pinchas Cohen from the University of Southern California, whose team published its findings this month told Thailand Medical News, "We knew that when the virus attacks cells, bad things happen but we didn't know why. Now we can say, when the virus attacks cells, it damages the mitochondria."
The study team found that the virus caused "dramatic changes and impairment" in the genes that regulate mitochondrial function.
The implication is that energy production in the cells and innate immunity are then impaired.
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