Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41467-017-02816-2
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dc.titleAn evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction
dc.contributor.authorXia, H
dc.contributor.authorLuo, H
dc.contributor.authorShan, C
dc.contributor.authorMuruato, A.E
dc.contributor.authorNunes, B.T.D
dc.contributor.authorMedeiros, D.B.A
dc.contributor.authorZou, J
dc.contributor.authorXie, X
dc.contributor.authorGiraldo, M.I
dc.contributor.authorVasconcelos, P.F.C
dc.contributor.authorWeaver, S.C
dc.contributor.authorWang, T
dc.contributor.authorRajsbaum, R
dc.contributor.authorShi, P.-Y
dc.date.accessioned2020-10-20T09:59:29Z
dc.date.available2020-10-20T09:59:29Z
dc.date.issued2018
dc.identifier.citationXia, 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
dc.identifier.issn2041-1723
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/178458
dc.description.abstractVirus-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.
dc.publisherNature Publishing Group
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectbeta interferon
dc.subjectinterferon regulatory factor 3
dc.subjectnonstructural protein 1
dc.subjectnonstructural protein 2A
dc.subjectnonstructural protein 2B
dc.subjectnonstructural protein 4A
dc.subjectnonstructural protein 4B
dc.subjectnonstructural protein 5
dc.subjectphosphotransferase
dc.subjectretinoic acid inducible protein I
dc.subjectTANK binding kinase 1
dc.subjectunclassified drug
dc.subjectviral protein
dc.subjectinterferon
dc.subjectNS1 protein, zika virus
dc.subjectprotein serine threonine kinase
dc.subjectTBK1 protein, human
dc.subjectantigen
dc.subjectepidemic
dc.subjectgene
dc.subjecthost-pathogen interaction
dc.subjectimmune response
dc.subjectmosquito
dc.subjectmutation
dc.subjectvirus
dc.subjectZika virus disease
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectcontrolled study
dc.subjectcytokine production
dc.subjectdendritic cell
dc.subjectenzyme phosphorylation
dc.subjectevolution
dc.subjectgene mutation
dc.subjectHEK293T cell line
dc.subjecthuman
dc.subjecthuman cell
dc.subjectinterferon induction
dc.subjectmouse
dc.subjectmRNA expression level
dc.subjectnewborn
dc.subjectnonhuman
dc.subjectpromoter region
dc.subjectprotein binding
dc.subjectprotein expression
dc.subjectprotein phosphorylation
dc.subjectprotein protein interaction
dc.subjectsurvival time
dc.subjectviremia
dc.subjectvirus cell interaction
dc.subjectvirus load
dc.subjectvirus replication
dc.subjectZika fever
dc.subjectgenetics
dc.subjectimmune evasion
dc.subjectimmunology
dc.subjectmolecular evolution
dc.subjectmutation
dc.subjectphylogeny
dc.subjectvirology
dc.subjectZika virus
dc.subjectZika virus
dc.subjectEvolution, Molecular
dc.subjectHumans
dc.subjectImmune Evasion
dc.subjectInterferons
dc.subjectMutation
dc.subjectPhylogeny
dc.subjectProtein-Serine-Threonine Kinases
dc.subjectViral Nonstructural Proteins
dc.subjectZika Virus
dc.subjectZika Virus Infection
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1038/s41467-017-02816-2
dc.description.sourcetitleNature Communications
dc.description.volume9
dc.description.issue1
dc.description.page414
dc.published.statepublished
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