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10.1016/j.celrep.2020.107940

http://scihub22266oqcxt.onion/10.1016/j.celrep.2020.107940
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suck abstract from ncbi


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pmid32668216      Cell+Rep 2020 ; 32 (3): 107940
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  • Remdesivir Inhibits SARS-CoV-2 in Human Lung Cells and Chimeric SARS-CoV Expressing the SARS-CoV-2 RNA Polymerase in Mice #MMPMID32668216
  • Pruijssers AJ; George AS; Schafer A; Leist SR; Gralinksi LE; Dinnon KH 3rd; Yount BL; Agostini ML; Stevens LJ; Chappell JD; Lu X; Hughes TM; Gully K; Martinez DR; Brown AJ; Graham RL; Perry JK; Du Pont V; Pitts J; Ma B; Babusis D; Murakami E; Feng JY; Bilello JP; Porter DP; Cihlar T; Baric RS; Denison MR; Sheahan TP
  • Cell Rep 2020[Jul]; 32 (3): 107940 PMID32668216show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the novel viral disease COVID-19. With no approved therapies, this pandemic illustrates the urgent need for broad-spectrum antiviral countermeasures against SARS-CoV-2 and future emerging CoVs. We report that remdesivir (RDV) potently inhibits SARS-CoV-2 replication in human lung cells and primary human airway epithelial cultures (EC(50) = 0.01 muM). Weaker activity is observed in Vero E6 cells (EC(50) = 1.65 muM) because of their low capacity to metabolize RDV. To rapidly evaluate in vivo efficacy, we engineered a chimeric SARS-CoV encoding the viral target of RDV, the RNA-dependent RNA polymerase of SARS-CoV-2. In mice infected with the chimeric virus, therapeutic RDV administration diminishes lung viral load and improves pulmonary function compared with vehicle-treated animals. These data demonstrate that RDV is potently active against SARS-CoV-2 in vitro and in vivo, supporting its further clinical testing for treatment of COVID-19.
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