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Title: Biology of Zika virus infection in human skin cells
Authors: Rodolphe Hamel
Ophélie Dejarnac
Sineewanlaya Wichit
Peeraya Ekchariyawat
Aymeric Neyret
Natthanej Luplertlop
Manuel Perera-Lecoin
Pornapat Surasombatpattana
Loïc Talignani
Frédéric Thomas
Van Mai Cao-Lormeau
Valérie Choumet
Laurence Briant
Philippe Desprès
Ali Amara
Hans Yssel
Dorothée Missé
Maladies Infectieuses et Vecteurs : Ecologie, Genetique, Evolution et Controle
CNRS Centre National de la Recherche Scientifique
Mahidol University
Prince of Songkla University
Institut Louis Malarde
Institut Pasteur, Paris
Universite de La Reunion
Keywords: Agricultural and Biological Sciences;Immunology and Microbiology
Issue Date: 1-Jan-2015
Citation: Journal of Virology. Vol.89, No.17 (2015), 8880-8896
Abstract: © 2015, American Society for Microbiology. Zika virus (ZIKV) is an emerging arbovirus of the Flaviviridae family, which includes dengue, West Nile, yellow fever, and Japanese encephalitis viruses, that causes a mosquito-borne disease transmitted by the Aedes genus, with recent outbreaks in the South Pacific. Here we examine the importance of human skin in the entry of ZIKV and its contribution to the induction of antiviral immune responses. We show that human dermal fibroblasts, epidermal keratinocytes, and immature dendritic cells are permissive to the most recent ZIKV isolate, responsible for the epidemic in French Polynesia. Several entry and/or adhesion factors, including DC-SIGN, AXL, Tyro3, and, to a lesser extent, TIM-1, permitted ZIKV entry, with a major role for the TAM receptor AXL. The ZIKV permissiveness of human skin fibroblasts was confirmed by the use of a neutralizing antibody and specific RNA silencing. ZIKV induced the transcription of Toll-like receptor 3 (TLR3), RIG-I, and MDA5, as well as several interferonstimulated genes, including OAS2, ISG15, and MX1, characterized by strongly enhanced beta interferon gene expression. ZIKV was found to be sensitive to the antiviral effects of both type I and type II interferons. Finally, infection of skin fibroblasts resulted in the formation of autophagosomes, whose presence was associated with enhanced viral replication, as shown by the use of Torin 1, a chemical inducer of autophagy, and the specific autophagy inhibitor 3-methyladenine. The results presented herein permit us to gain further insight into the biology of ZIKV and to devise strategies aiming to interfere with the pathology caused by this emerging flavivirus.
ISSN: 10985514
Appears in Collections:Scopus 2011-2015

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