This study demonstrates that Favipiravir's antiviral effect against SARS-CoV-2 primarily stems from lethal mutagenesis. The SARS-CoV RdRp complex, exhibiting exceptionally high activity and error rates, readily incorporates Favipiravir into viral RNA, inducing C-to-U and G-to-A mutations. This high incorporation rate, coupled with the low cytosine content of the SARS-CoV-2 genome, leads to significant genomic instability and viral inhibition.
Publisher
Nature Communications
Published On
Sep 17, 2020
Authors
Ashleigh Shannon, Barbara Selisko, Nhung-Thi-Tuyet Le, Johanna Huchting, Franck Touret, Géraldine Piorkowski, Véronique Fattorini, François Ferron, Etienne Decroly, Chris Meier, Bruno Coutard, Olve Peersen, Bruno Canard
Tags
Favipiravir
SARS-CoV-2
antiviral
lethal mutagenesis
genomic instability
viral inhibition
RNA mutations
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