Zika Virus NS3 Mimics a Cellular 14-3-3-Binding Motif to Antagonize RIG-I- and MDA5-Mediated Innate Immunity.

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ID: 60322
2019
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Abstract
14-3-3 protein family members facilitate the translocation of RIG-I-like receptors (RLRs) to organelles that mediate downstream RLR signaling, leading to interferon production. 14-3-3ϵ promotes the cytosolic-to-mitochondrial translocation of RIG-I, while 14-3-3η facilitates MDA5 translocation to mitochondria. We show that the NS3 protein of Zika virus (ZIKV) antagonizes antiviral gene induction by RIG-I and MDA5 by binding to and sequestering the scaffold proteins 14-3-3ϵ and 14-3-3η. 14-3-3-binding is mediated by a negatively charged RLDP motif in NS3 that is conserved in ZIKV strains of African and Asian lineages and is similar to the one found in dengue and West Nile viruses. ZIKV NS3 is sufficient to inhibit the RLR-14-3-3ϵ/η interaction and to suppress antiviral signaling. Mutational perturbation of 14-3-3ϵ/η binding in a recombinant ZIKV leads to enhanced innate immune responses and impaired growth kinetics. Our study provides molecular understanding of immune evasion functions of ZIKV, which may guide vaccine and anti-flaviviral therapy development.
Reference Key
riedl2019zikacell Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Riedl, William;Acharya, Dhiraj;Lee, Jung-Hyun;Liu, Guanqun;Serman, Taryn;Chiang, Cindy;Chan, Ying Kai;Diamond, Michael S;Gack, Michaela U;
Journal cell host & microbe
Year 2019
DOI
S1931-3128(19)30479-2
URL
Keywords
zika virus innate immunity interferon rig-i-like receptors flaviviruses viral immune evasion

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