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  • DDX56 antoginizes IFN-β production to enhance EMCV replication by inhibiting IRF3 nuclear translocation

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    Idris526087-Accepted.pdf (3.470Mb)
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    Accepted Manuscript (AM)
    Author(s)
    Xu, Shujuan
    Xie, Jingying
    Zhang, Xiangbo
    Chen, Lei
    Bi, Yingjie
    Li, Xiangrong
    Idris, Adi
    Feng, Ruofei
    Griffith University Author(s)
    Idris, Adi
    Year published
    2022
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    Abstract
    DEAD (Asp-Glu-Ala-Asp)-box RNA helicases (DDX) play important roles in viral infection, either as cytosolic viral nucleic acids sensors or as essential host factors for viral replication. In this study, we identified DDX56 as a positive regulator for encephalomyocarditis virus (EMCV) replication. EMCV infection promotes DDX56 expression via its viral proteins, VP3 and 3C. We showed that DDX56 overexpression promotes EMCV replication whereas its loss dampened EMCV replication. Consequently, knockdown of DDX56 increases type I interferon (IFN) expression during EMCV infection. We also showed that DDX56 interrupts IFN regulatory ...
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    DEAD (Asp-Glu-Ala-Asp)-box RNA helicases (DDX) play important roles in viral infection, either as cytosolic viral nucleic acids sensors or as essential host factors for viral replication. In this study, we identified DDX56 as a positive regulator for encephalomyocarditis virus (EMCV) replication. EMCV infection promotes DDX56 expression via its viral proteins, VP3 and 3C. We showed that DDX56 overexpression promotes EMCV replication whereas its loss dampened EMCV replication. Consequently, knockdown of DDX56 increases type I interferon (IFN) expression during EMCV infection. We also showed that DDX56 interrupts IFN regulatory factor 3 (IRF3) phosphorylation and its nucleus translocation by directly targeting KPNA3 and KPNA4 in an EMCV-triggered MDA5 signaling activation cascade leading to the blockade of IFN-β production. Overall, we showed that DDX56 is a novel negative regulator of EMCV-mediated IFN-β responses and that DDX56 plays a critical role in EMCV replication. These findings reveal a novel strategy for EMCV to utilize a host factor to evade the host innate immune response and provide us new insight into the function of DDX56.
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    Journal Title
    Veterinary Microbiology
    Volume
    264
    DOI
    https://doi.org/10.1016/j.vetmic.2021.109304
    Copyright Statement
    © 2022 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
    Subject
    Microbiology
    Veterinary sciences
    Publication URI
    http://hdl.handle.net/10072/411509
    Collection
    • Journal articles

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