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Virology. 2016 Jun;493:217-26. doi: 10.1016/j.virol.2016.03.006. Epub 2016 Apr 6.

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

Author information

1
Université de la Réunion, UM 134 Processus Infectieux en Milieu Insulaire Tropical (PIMIT), INSERM U1187, CNRS UMR9192, IRD UMR249. Plateforme Technologique CYROI, 97490 Sainte Clotilde, France.
2
Université de la Réunion, UMR Diabète Athérothrombose Thérapies Réunion Océan Indien (DeTROI), INSERM U1188, Plateforme Technologique CYROI, 97490 Sainte Clotilde, France.
3
Laboratoire MIVEGEC, UMR 224 IRD/CNRS/UM, 34394 Montpellier, France.
4
Université de la Réunion, UM 134 Processus Infectieux en Milieu Insulaire Tropical (PIMIT), INSERM U1187, CNRS UMR9192, IRD UMR249. Plateforme Technologique CYROI, 97490 Sainte Clotilde, France. Electronic address: wildriss.viranaicken@univ-reunion.fr.
5
Université de la Réunion, UM 134 Processus Infectieux en Milieu Insulaire Tropical (PIMIT), INSERM U1187, CNRS UMR9192, IRD UMR249. Plateforme Technologique CYROI, 97490 Sainte Clotilde, France. Electronic address: philippe.despres@univ-reunion.fr.

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.

KEYWORDS:

Apoptosis; Arbovirus; Emerging virus; Human epithelial cells; Innate immunity; Oxidative stress; Type-I interferon; Viral pathogenicity; Zika virus

PMID:
27060565
DOI:
10.1016/j.virol.2016.03.006
[Indexed for MEDLINE]
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