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An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction

Author

Listed:
  • Hongjie Xia

    (University of Texas Medical Branch)

  • Huanle Luo

    (University of Texas Medical Branch)

  • Chao Shan

    (University of Texas Medical Branch)

  • Antonio E. Muruato

    (University of Texas Medical Branch
    University of Texas Medical Branch)

  • Bruno T. D. Nunes

    (University of Texas Medical Branch
    Ministry of Health)

  • Daniele B. A. Medeiros

    (University of Texas Medical Branch
    Ministry of Health)

  • Jing Zou

    (University of Texas Medical Branch)

  • Xuping Xie

    (University of Texas Medical Branch)

  • Maria Isabel Giraldo

    (University of Texas Medical Branch)

  • Pedro F. C. Vasconcelos

    (Ministry of Health
    Pará State University)

  • Scott C. Weaver

    (University of Texas Medical Branch
    University of Texas Medical Branch
    University of Texas Medical Branch
    University of Texas Medical Branch)

  • Tian Wang

    (University of Texas Medical Branch
    University of Texas Medical Branch
    University of Texas Medical Branch)

  • Ricardo Rajsbaum

    (University of Texas Medical Branch
    University of Texas Medical Branch)

  • Pei-Yong Shi

    (University of Texas Medical Branch
    University of Texas Medical Branch
    University of Texas Medical Branch
    University of Texas Medical Branch)

Abstract

Virus–host interactions determine an infection outcome. The Asian lineage of Zika virus (ZIKV), responsible for the recent epidemics, has fixed a mutation in the NS1 gene after 2012 that enhances mosquito infection. Here we report that the same mutation confers NS1 to inhibit interferon-β induction. This mutation enables NS1 binding to TBK1 and reduces TBK1 phosphorylation. Engineering the mutation into a pre-epidemic ZIKV strain debilitates the virus for interferon-β induction; reversing the mutation in an epidemic ZIKV strain invigorates the virus for interferon-β induction; these mutational effects are lost in IRF3-knockout cells. Additionally, ZIKV NS2A, NS2B, NS4A, NS4B, and NS5 can also suppress interferon-β production through targeting distinct components of the RIG-I pathway; however, for these proteins, no antagonistic difference is observed among various ZIKV strains. Our results support the mechanism that ZIKV has accumulated mutation(s) that increases the ability to evade immune response and potentiates infection and epidemics.

Suggested Citation

  • Hongjie Xia & Huanle Luo & Chao Shan & Antonio E. Muruato & Bruno T. D. Nunes & Daniele B. A. Medeiros & Jing Zou & Xuping Xie & Maria Isabel Giraldo & Pedro F. C. Vasconcelos & Scott C. Weaver & Tian, 2018. "An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
  • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02816-2
    DOI: 10.1038/s41467-017-02816-2
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    Cited by:

    1. Jimena Barbeito-Andrés & Lavínia Schuler-Faccini & Patricia Pestana Garcez, 2018. "Why is congenital Zika syndrome asymmetrically distributed among human populations?," PLOS Biology, Public Library of Science, vol. 16(8), pages 1-11, August.

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