Scientific reports · 2017
The clinically approved antiviral drug sofosbuvir inhibits Zika virus replication.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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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, de Mello Volotão Eduardo, 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, Souza Thiago Moreno L
Аннотация
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.