Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41467-017-02816-2
Title: An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction
Authors: Xia, H
Luo, H
Shan, C
Muruato, A.E
Nunes, B.T.D
Medeiros, D.B.A
Zou, J
Xie, X
Giraldo, M.I
Vasconcelos, P.F.C
Weaver, S.C
Wang, T
Rajsbaum, R
Shi, P.-Y 
Keywords: beta interferon
interferon regulatory factor 3
nonstructural protein 1
nonstructural protein 2A
nonstructural protein 2B
nonstructural protein 4A
nonstructural protein 4B
nonstructural protein 5
phosphotransferase
retinoic acid inducible protein I
TANK binding kinase 1
unclassified drug
viral protein
interferon
NS1 protein, zika virus
protein serine threonine kinase
TBK1 protein, human
antigen
epidemic
gene
host-pathogen interaction
immune response
mosquito
mutation
virus
Zika virus disease
animal experiment
animal model
Article
controlled study
cytokine production
dendritic cell
enzyme phosphorylation
evolution
gene mutation
HEK293T cell line
human
human cell
interferon induction
mouse
mRNA expression level
newborn
nonhuman
promoter region
protein binding
protein expression
protein phosphorylation
protein protein interaction
survival time
viremia
virus cell interaction
virus load
virus replication
Zika fever
genetics
immune evasion
immunology
molecular evolution
mutation
phylogeny
virology
Zika virus
Zika virus
Evolution, Molecular
Humans
Immune Evasion
Interferons
Mutation
Phylogeny
Protein-Serine-Threonine Kinases
Viral Nonstructural Proteins
Zika Virus
Zika Virus Infection
Issue Date: 2018
Publisher: Nature Publishing Group
Citation: Xia, H, Luo, H, Shan, C, Muruato, A.E, Nunes, B.T.D, Medeiros, D.B.A, Zou, J, Xie, X, Giraldo, M.I, Vasconcelos, P.F.C, Weaver, S.C, Wang, T, Rajsbaum, R, Shi, P.-Y (2018). An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction. Nature Communications 9 (1) : 414. ScholarBank@NUS Repository. https://doi.org/10.1038/s41467-017-02816-2
Rights: Attribution 4.0 International
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-? 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-? induction; reversing the mutation in an epidemic ZIKV strain invigorates the virus for interferon-? induction; these mutational effects are lost in IRF3-knockout cells. Additionally, ZIKV NS2A, NS2B, NS4A, NS4B, and NS5 can also suppress interferon-? 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. © The Author(s) 2018.
Source Title: Nature Communications
URI: https://scholarbank.nus.edu.sg/handle/10635/178458
ISSN: 2041-1723
DOI: 10.1038/s41467-017-02816-2
Rights: Attribution 4.0 International
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