The South Pacific epidemic strain of Zika virus replicates efficiently in human epithelial A549 cells leading to IFN-β production and apoptosis induction

Abstract 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...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2016-06, Vol.493, p.217-226
Main Authors: Frumence, Etienne, Roche, Marjolaine, Krejbich-Trotot, Pascale, El-Kalamouni, Chaker, Nativel, Brice, Rondeau, Philippe, Missé, Dorothée, Gadea, Gilles, Viranaicken, Wildriss, Desprès, Philippe
Format: Article
Language:English
Subjects:
A549 Cells
Alveolar Epithelial Cells - metabolism
Alveolar Epithelial Cells - virology
Animals
Apoptosis
Arbovirus
Autophagy
Cercopithecus aethiops
Cytokines - biosynthesis
Emerging virus
Flavivirus
Human epithelial cells
Humans
Infectious Disease
Innate immunity
Interferon-beta - biosynthesis
Interferon-beta - genetics
Interferon-beta - secretion
Life Sciences
Microbiology and Parasitology
Mitochondria
Oxidative stress
Type-I interferon
Vero Cells
Viral pathogenicity
Virology
Virus Replication
Zika virus
Zika Virus - physiology
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Summary:Abstract 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-β followed by the expression of pro-inflammatory cytokines such as IL-1β, 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-β which exerts an antiviral effect against ZIKV might delay apoptosis in infected cells.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2016.03.006