1. Corrigendum: The clinically approved antiviral drug sofosbuvir inhibits Zika virus replication
- Author
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Sacramento, Carolina Q., de Melo, Gabrielle R., de Freitas, Caroline S., Rocha, Natasha, Hoelz, Lucas Villas Bôas, Miranda, Milene, Fintelman-Rodrigues, Natalia, Marttorelli, Andressa, Ferreira, André C., Barbosa-Lima, Giselle, Abrantes, Juliana L., Vieira, Yasmine Rangel, Bastos, Mônica M., Volotão, Eduardo de Mello, Nunes, Estevão Portela, Tschoeke, Diogo A., Leomil, Luciana, Loiola, Erick Correia, Trindade, Pablo, Rehen, Stevens K., Bozza, Fernando A., Bozza, Patrícia T., Boechat, Nubia, Thompson, Fabiano L., de Filippis, Ana M. B., Brüning, Karin, and Souza, Thiago Moreno L.
- Subjects
Cell Survival ,Zika Virus Infection ,viruses ,DNA-Directed RNA Polymerases ,Genome, Viral ,Zika Virus ,Virus Replication ,Corrigenda ,Antiviral Agents ,Article ,Cell Line ,Viral Proteins ,Mutation ,Humans ,Sofosbuvir - Abstract
Zika virus (ZIKV) is a member of the Flaviviridae family, along with other agents of clinical significance such as dengue (DENV) and hepatitis C (HCV) viruses. Since ZIKV causes neurological disorders during fetal development and in adulthood, antiviral drugs are necessary. Sofosbuvir is clinically approved for use against HCV and targets the protein that is most conserved among the members of the Flaviviridae family, the viral RNA polymerase. Indeed, we found that sofosbuvir inhibits ZIKV RNA polymerase, targeting conserved amino acid residues. Sofosbuvir inhibited ZIKV replication in different cellular systems, such as hepatoma (Huh-7) cells, neuroblastoma (SH-Sy5y) cells, neural stem cells (NSC) and brain organoids. In addition to the direct inhibition of the viral RNA polymerase, we observed that sofosbuvir also induced an increase in A-to-G mutations in the viral genome. Together, our data highlight a potential secondary use of sofosbuvir, an anti-HCV drug, against ZIKV.
- Published
- 2017