Journal
VIROLOGY
Volume 493, Issue -, Pages 217-226Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2016.03.006
Keywords
Zika virus; Arbovirus; Emerging virus; Viral pathogenicity; Apoptosis; Oxidative stress; Innate immunity; Type-I interferon; Human epithelial cells
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Funding
- Agence Nationale de la Recherche, France [ANR-12-BSV3-0004-01]
- Conseil Regional de l'Ile de La Reunion, France [DIRED 20121399, DIRED 20131515]
- Agence Nationale de la Recherche (ANR) [ANR-12-BSV3-0004] Funding Source: Agence Nationale de la Recherche (ANR)
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Zika virus (ZIKV) is an emerging flavivirus since the first epidemics in South Pacific in 2007. The recent finding that ZIKV is now circulating in Western Hemisphere and can be associated to severe human diseases, warrants the need for its study. Here we evaluate the susceptibility of human lung epithelial A549 cells to South Pacific epidemic strain of ZIKV isolated in 2013. We showed that ZIKV growth in A549 cells is greatly efficient. ZIKV infection resulted in the secretion of IFN-beta followed by the expression of pro-inflammatory cytokines such as IL-1 beta, and transcriptional activity of IFIT genes. At the maximum of virus progeny production, ZIKV triggers mitochondrial apoptosis through activation of caspases-3 and -9. Whereas at early infection times, the rapid release of IFN-1 beta which exerts an antiviral effect against ZIKV might delay apoptosis in infected cells. (C) 2016 Elsevier Inc. All rights reserved.
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