Journal
CELL REPORTS
Volume 32, Issue 3, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.107940
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Funding
- National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services [1U19AI142759, R01AI132178, R01AI132178-03S1, R01AI108197]
- Burroughs Wellcome Fund Postdoctoral Enrichment Program award
- NIH [DK065988]
- Cystic Fibrosis Foundation grant [BOUCHE15RO]
- Dolly Parton COVID-19 Research Fund
- VUMC Office of Research
- Elizabeth B. Lamb Center for Pediatric Research at Vanderbilt University
- [T32AI007151]
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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 (EC50 = 0.01 mu M). Weaker activity is observed in Vero E6 cells (EC50 = 1.65 mu M) 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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