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Evasion of Innate and Intrinsic Antiviral Pathways by the Zika Virus

Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA
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Author to whom correspondence should be addressed.
Viruses 2019, 11(10), 970; https://doi.org/10.3390/v11100970
Received: 29 September 2019 / Revised: 19 October 2019 / Accepted: 20 October 2019 / Published: 22 October 2019
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
The Zika virus (ZIKV) is a recently emerged mosquito-borne flavivirus that, while typically asymptomatic, can cause neurological symptoms in adults and birth defects in babies born to infected mothers. The interactions of ZIKV with many different pathways in the human host ultimately determine successful virus replication and ZIKV-induced pathogenesis; however, the molecular mechanisms of such host-ZIKV interactions have just begun to be elucidated. Here, we summarize the recent advances that defined the mechanisms by which ZIKV antagonizes antiviral innate immune signaling pathways, with a particular focus on evasion of the type I interferon response in the human host. Furthermore, we describe emerging evidence that indicated the contribution of several cell-intrinsic mechanisms to an effective restriction of ZIKV infection, such as nonsense-mediated mRNA decay, stress granule formation, and “reticulophagy”, a type of selective autophagy. Finally, we summarize the recent work that identified strategies by which ZIKV modulated these intrinsic antiviral responses. View Full-Text
Keywords: flavivirus; Zika virus; innate immunity; antiviral; interferon; stress response; nonsense-mediated mRNA Decay; autophagy flavivirus; Zika virus; innate immunity; antiviral; interferon; stress response; nonsense-mediated mRNA Decay; autophagy
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Serman, T.M.; Gack, M.U. Evasion of Innate and Intrinsic Antiviral Pathways by the Zika Virus. Viruses 2019, 11, 970.

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