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      The Antiviral Drug Arbidol Inhibits Zika Virus

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          Abstract

          There are many emerging and re-emerging globally prevalent viruses for which there are no licensed vaccines or antiviral medicines. Arbidol (ARB, umifenovir), used clinically for decades in several countries as an anti-influenza virus drug, inhibits many other viruses. In the current study, we show that ARB inhibits six different isolates of Zika virus (ZIKV), including African and Asian lineage viruses in multiple cell lines and primary human vaginal and cervical epithelial cells. ARB protects against ZIKV-induced cytopathic effects. Time of addition studies indicate that ARB is most effective at suppressing ZIKV when added to cells prior to infection. Moreover, ARB inhibits pseudoviruses expressing the ZIKV Envelope glycoprotein. Thus, ARB, a broadly acting anti-viral agent with a well-established safety profile, inhibits ZIKV, likely by blocking viral entry.

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          Most cited references34

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          Robust hepatitis C virus infection in vitro.

          The absence of a robust cell culture model of hepatitis C virus (HCV) infection has severely limited analysis of the HCV life cycle and the development of effective antivirals and vaccines. Here we report the establishment of a simple yet robust HCV cell culture infection system based on the HCV JFH-1 molecular clone and Huh-7-derived cell lines that allows the production of virus that can be efficiently propagated in tissue culture. This system provides a powerful tool for the analysis of host-virus interactions that should facilitate the discovery of antiviral drugs and vaccines for this important human pathogen.
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            Vaginal Exposure to Zika Virus during Pregnancy Leads to Fetal Brain Infection.

            Zika virus (ZIKV) can be transmitted sexually between humans. However, it is unknown whether ZIKV replicates in the vagina and impacts the unborn fetus. Here, we establish a mouse model of vaginal ZIKV infection and demonstrate that, unlike other routes, ZIKV replicates within the genital mucosa even in wild-type (WT) mice. Mice lacking RNA sensors or transcription factors IRF3 and IRF7 resulted in higher levels of local viral replication. Furthermore, mice lacking the type I interferon (IFN) receptor (IFNAR) became viremic and died of infection after a high-dose vaginal ZIKV challenge. Notably, vaginal infection of pregnant dams during early pregnancy led to fetal growth restriction and infection of the fetal brain in WT mice. This was exacerbated in mice deficient in IFN pathways, leading to abortion. Our study highlights the vaginal tract as a highly susceptible site of ZIKV replication and illustrates the dire disease consequences during pregnancy.
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              Zika virus infection complicated by Guillain-Barré syndrome – case report, French Polynesia, December 2013

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                Author and article information

                Contributors
                polyak@uw.edu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                12 June 2018
                12 June 2018
                2018
                : 8
                : 8989
                Affiliations
                [1 ]ISNI 0000000122986657, GRID grid.34477.33, Department of Laboratory Medicine, , University of Washington, ; Seattle, Washington USA
                [2 ]ISNI 0000000122986657, GRID grid.34477.33, Department of Obstetrics and Gynecology, , University of Washington, ; Seattle, Washington USA
                [3 ]ISNI 0000 0004 1936 7400, GRID grid.256304.6, Center for Microbial Pathogenesis, , Institute for Biomedical Sciences, Georgia State University, ; Atlanta, USA
                Author information
                http://orcid.org/0000-0003-1705-0103
                http://orcid.org/0000-0003-2343-0719
                Article
                27224
                10.1038/s41598-018-27224-4
                5997637
                29895962
                4a303b1e-ae8a-433f-bace-df12acf2f1a1
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 29 January 2018
                : 25 May 2018
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