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10.1101/2022.02.19.481089

http://scihub22266oqcxt.onion/10.1101/2022.02.19.481089
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35233572!8887073!35233572
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suck abstract from ncbi


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pmid35233572      bioRxiv 2022 ; ä (ä): ä
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  • TARGETED DOWN REGULATION OF CORE MITOCHONDRIAL GENES DURING SARS-COV-2 INFECTION #MMPMID35233572
  • Guarnieri JW; Dybas JM; Fazelinia H; Kim MS; Frere J; Zhang Y; Albrecht YS; Murdock DG; Angelin A; Singh LN; Weiss SL; Best SM; Lott MT; Cope H; Zaksas V; Saravia-Butler A; Meydan C; Foox J; Mozsary C; Kidane YH; Priebe W; Emmett MR; Meller R; Singh U; Bram Y; tenOever BR; Heise MT; Moorman NJ; Madden EA; Taft-Benz SA; Anderson EJ; Sanders WA; Dickmander RJ; Baxter VK; Baylin SB; Wurtele ES; Moraes-Vieira PM; Taylor D; Mason CE; Schisler JC; Schwartz RE; Beheshti A; Wallace DC
  • bioRxiv 2022[Feb]; ä (ä): ä PMID35233572show ga
  • Defects in mitochondrial oxidative phosphorylation (OXPHOS) have been reported in COVID-19 patients, but the timing and organs affected vary among reports. Here, we reveal the dynamics of COVID-19 through transcription profiles in nasopharyngeal and autopsy samples from patients and infected rodent models. While mitochondrial bioenergetics is repressed in the viral nasopharyngeal portal of entry, it is up regulated in autopsy lung tissues from deceased patients. In most disease stages and organs, discrete OXPHOS functions are blocked by the virus, and this is countered by the host broadly up regulating unblocked OXPHOS functions. No such rebound is seen in autopsy heart, results in severe repression of genes across all OXPHOS modules. Hence, targeted enhancement of mitochondrial gene expression may mitigate the pathogenesis of COVID-19.
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