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

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 Wang, Ricardo Rajsbaum and Pei-Yong Shi ()
Additional contact information
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
Bruno T. D. Nunes: University of Texas Medical Branch
Daniele B. A. Medeiros: University of Texas Medical Branch
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
Scott C. Weaver: University of Texas Medical Branch
Tian Wang: University of Texas Medical Branch
Ricardo Rajsbaum: University of Texas Medical Branch
Pei-Yong Shi: University of Texas Medical Branch

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-017-02816-2

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