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

被引：242

作者：

Xia, Hongjie ^{[1
]}

Luo, Huanle ^{[2
]}

Shan, Chao ^{[1
]}

Muruato, Antonio E. ^{[1
,2
]}

Nunes, Bruno T. D. ^{[1
,3
]}

Medeiros, Daniele B. A. ^{[1
,3
]}

Zou, Jing ^{[1
]}

Xie, Xuping ^{[1
]}

Giraldo, Maria Isabel ^{[2
]}

Vasconcelos, Pedro F. C. ^{[3
,4
]}

Weaver, Scott C. ^{[2
,5
,6
,7
,8
]}

Wang, Tian ^{[2
,7
,9
]}

Rajsbaum, Ricardo ^{[2
,5
]}

Shi, Pei-Yong ^{[1
,5
,6
,7
,8
,10
]}

机构：

[1] Univ Texas Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA

[2] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA

[3] Minist Hlth, Evandro Chagas Inst, Dept Arbovirol & Hemorrhag Fevers, Ananindeua, Para, Brazil

[4] Para State Univ, Dept Pathol, Belem, Para, Brazil

[5] Univ Texas Med Branch, Inst Human Infect & Immun, Galveston, TX 77555 USA

[6] Univ Texas Med Branch, Inst Translat Sci, Galveston, TX 77555 USA

[7] Univ Texas Med Branch, Sealy Ctr Vaccine Dev, Galveston, TX 77555 USA

[8] Univ Texas Med Branch, Sealy Ctr Struct Biol & Mol Biophys, Galveston, TX 77555 USA

[9] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA

[10] Univ Texas Med Branch, Dept Phamarcol & Toxicol, Galveston, TX 77555 USA

来源：

NATURE COMMUNICATIONS | 2018年 / 9卷

关键词：

WEST-NILE-VIRUS; DENGUE VIRUS; I INTERFERON; RIG-I; STIMULATED GENES; PROTEIN; PATHOGENESIS; IMMUNITY; RECOGNITION; INHIBITION;

D O I：

10.1038/s41467-017-02816-2

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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-beta 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-beta induction; reversing the mutation in an epidemic ZIKV strain invigorates the virus for interferon-beta induction; these mutational effects are lost in IRF3-knockout cells. Additionally, ZIKV NS2A, NS2B, NS4A, NS4B, and NS5 can also suppress interferon-beta 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.

引用

页数：13

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