Favipiravir and ribavirin inhibit replication of Asian and African strains of zika virus in different cell models

Ji Ae Kim, Rak Kyun Seong, Mukesh Kumar, Ok Sarah Shin

Research output: Contribution to journalArticlepeer-review

58 Citations (Scopus)

Abstract

Zika virus (ZIKV) has recently emerged as a new public health threat. ZIKV infections have caused a wide spectrum of neurological diseases, such as Guillain–Barré syndrome, myelitis, meningoencephalitis, and congenital microcephaly. No effective therapies currently exist for treating patients infected with ZIKV. Herein, we evaluated the anti-viral activity of favipiravir (T-705) and ribavirin against Asian and African strains of ZIKV using different cell models, including human neuronal progenitor cells (hNPCs), human dermal fibroblasts (HDFs), human lung adenocarcinoma cells (A549) and Vero cells. Cells were treated with favipiravir or ribavirin and effects on ZIKV replication were determined using quantitative real-time PCR and plaque assay. Our results demonstrate that favipiravir or ribavirin treatment significantly inhibited ZIKV replication in a dose-dependent manner. Moreover, favipiravir treatment of ZIKV-infected hNPCs led to reduced cell death, enhanced AKT pathway phosphorylation, and increased expression of anti-apoptotic factor B cell lymphoma 2. In conclusion, our results demonstrate conclusively that favipiravir inhibits ZIKV replication and prevents cell death, and can be a promising intervention for ZIKV-associated disease.

Original languageEnglish
Article number72
JournalViruses
Volume10
Issue number2
DOIs
Publication statusPublished - 2018 Feb 9
Externally publishedYes

Bibliographical note

Funding Information:
Acknowledgments: We would like to thank Ho-Seok Song (Korea University School of Medicine) for providing hNPC and Vincent Racaneillo (Columbia University, New York, NY, USA) for providing the ZIKV plaque assay protocol. This research was supported by the Basic Science Research Program of the National Research Foundation of Korea (NRF), Ministry of Science, ICT & Future Planning (NRF-2016R1C1B2006493). M.K. is supported by a grant (P30GM114737) from the Centers of Biomedical Research Excellence, National Institute of General Medical Sciences, grant (R21NS099838) from National Institute of Neurological Disorders and Stroke, and grant (R21OD024896) from the Office of the Director, National Institutes of Health.

Funding Information:
We would like to thank Ho-Seok Song (Korea University School of Medicine) for providing hNPC and Vincent Racaneillo (Columbia University, New York, NY, USA) for providing the ZIKV plaque assay protocol. This research was supported by the Basic Science Research Program of the National Research Foundation of Korea (NRF), Ministry of Science, ICT & Future Planning (NRF-2016R1C1B2006493). M.K. is supported by a grant (P30GM114737) from the Centers of Biomedical Research Excellence, National Institute of General Medical Sciences, grant (R21NS099838) from National Institute of Neurological Disorders and Stroke, and grant (R21OD024896) from the Office of the Director, National Institutes of Health.

Publisher Copyright:
© 2018 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

  • Anti-viral
  • Favipiravir
  • HNPCs
  • Ribavirin
  • Zika virus

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

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