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

xmlui.dri2xhtml.METS-1.0.item-date
2018xmlui.dri2xhtml.METS-1.0.item-files-viewOpen
xmlui.mirage2.itemSummaryView.MetaData
xmlui.ArtifactBrowser.ItemViewer.show_fullxmlui.dri2xhtml.METS-1.0.item-uri
http://patua.iec.gov.br//handle/iec/3060xmlui.dri2xhtml.METS-1.0.item-author
Xia, Hongjie
Luo, Huanle
Shan, Chao
Muruato, Antonio E
Nunes, Bruno Tardelli Diniz
Medeiros, Daniele Barbosa de Almeida
Zou, Jing
Xie, Xuping
Giraldo, Maria Isabel
Vasconcelos, Pedro Fernando da Costa
Weaver, Scott C
Wang, Tian
Rajsbaum, Ricardo
Shi, Pei-Yong
xmlui.dri2xhtml.METS-1.0.item-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.
xmlui.dri2xhtml.METS-1.0.item-citation
XIA, Hongjie et al. An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction. Nature Communications, v. 9, n. 1, p. 1-13, Jan. 2018.xmlui.dri2xhtml.METS-1.0.item-decsPrimary
Zika virus / patogenicidadeInfecção pelo Zika virus / diagnóstico
Interações Hospedeiro-Parasita / imunologia
Mutagênese / imunologia