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      Zika virus induces strong inflammatory responses and impairs homeostasis and function of the human retinal pigment epithelium

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          Abstract

          Background

          Zika virus (ZIKV) has recently re-emerged as a pathogenic agent with epidemic capacities as was well illustrated in South America. Because of the extent of this health crisis, a number of more serious symptoms have become associated with ZIKV infection than what was initially described. In particular, neuronal and ocular disorders have been characterized, both in infants and in adults. Notably, the macula and the retina can be strongly affected by ZIKV, possibly by a direct effect of the virus. This is supported by the detection of replicative and infectious virus in lachrimal fluid in human patients and mouse models.

          Methods

          Here, we used an innovative, state-of-the-art iPSC-derived human retinal pigment epithelium (RPE) model to study ZIKV retinal impairment.

          Findings

          We showed that the human RPE is highly susceptible to ZIKV infection and that a ZIKV African strain was more virulent and led to a more potent epithelium disruption and stronger anti-viral response than an Asian strain, suggesting lineage differences. Moreover, ZIKV infection led to impaired membrane dynamics involved in endocytosis, organelle biogenesis and potentially secretion, key mechanisms of RPE homeostasis and function.

          Interpretation

          Taken together, our results suggest that ZIKV has a highly efficient ocular tropism, which creates a strong inflammatory environment that could have acute or chronic adverse effects.

          Fund

          This work was funded by Retina France, REACTing and La Région Languedoc-Roussillon.

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          Most cited references 102

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          Interferon-stimulated genes: a complex web of host defenses.

          Interferon-stimulated gene (ISG) products take on a number of diverse roles. Collectively, they are highly effective at resisting and controlling pathogens. In this review, we begin by introducing interferon (IFN) and the JAK-STAT signaling pathway to highlight features that impact ISG production. Next, we describe ways in which ISGs both enhance innate pathogen-sensing capabilities and negatively regulate signaling through the JAK-STAT pathway. Several ISGs that directly inhibit virus infection are described with an emphasis on those that impact early and late stages of the virus life cycle. Finally, we describe ongoing efforts to identify and characterize antiviral ISGs, and we provide a forward-looking perspective on the ISG landscape.
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            Zika virus. I. Isolations and serological specificity.

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              Is Open Access

              Potential Sexual Transmission of Zika Virus

              In December 2013, during a Zika virus (ZIKV) outbreak in French Polynesia, a patient in Tahiti sought treatment for hematospermia, and ZIKV was isolated from his semen. ZIKV transmission by sexual intercourse has been previously suspected. This observation supports the possibility that ZIKV could be transmitted sexually.
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                Author and article information

                Contributors
                Journal
                EBioMedicine
                EBioMedicine
                EBioMedicine
                Elsevier
                2352-3964
                20 December 2018
                January 2019
                20 December 2018
                : 39
                : 315-331
                Affiliations
                [a ]Pathogenesis and Control of Chronic Infections, INSERM, Etablissement Français du Sang, University of Montpellier, Montpellier, France
                [b ]Institute for Neurosciences of Montpellier, INSERM, University of Montpellier, Montpellier, France
                [c ]BioCommunication en CardioMétabolique, University of Montpellier, Montpellier, France
                [d ]Pathogenesis and Control of Chronic Infections. INSERM, University of Montpellier, Etablissement Français du Sang, CHU Montpellier, Montpellier, France
                Author notes
                [1]

                Equally contributed.

                [2]

                Co-last authors.

                S2352-3964(18)30581-4
                10.1016/j.ebiom.2018.12.010
                6354710
                30579862
                © 2018 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                Categories
                Research paper

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