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dc.contributor.authorXia, Hongjie-
dc.contributor.authorLuo, Huanle-
dc.contributor.authorShan, Chao-
dc.contributor.authorMuruato, Antonio E-
dc.contributor.authorNunes, Bruno Tardelli Diniz-
dc.contributor.authorMedeiros, Daniele Barbosa de Almeida-
dc.contributor.authorZou, Jing-
dc.contributor.authorXie, Xuping-
dc.contributor.authorGiraldo, Maria Isabel-
dc.contributor.authorVasconcelos, Pedro Fernando da Costa-
dc.contributor.authorWeaver, Scott C-
dc.contributor.authorWang, Tian-
dc.contributor.authorRajsbaum, Ricardo-
dc.contributor.authorShi, Pei-Yong-
dc.date.accessioned2018-02-28T18:32:54Z-
dc.date.available2018-02-28T18:32:54Z-
dc.date.issued2018-
dc.identifier.citationXIA, 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.pt_BR
dc.identifier.issn2041-1723-
dc.identifier.urihttp://patua.iec.gov.br//handle/iec/3060-
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-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.pt_BR
dc.language.isoengpt_BR
dc.publisherNature Publishing Grouppt_BR
dc.rightsAcesso Abertopt_BR
dc.titleAn evolutionary NS1 mutation enhances Zika virus evasion of host interferon inductionpt_BR
dc.typeArtigopt_BR
dc.subject.decsPrimaryZika virus / patogenicidadept_BR
dc.subject.decsPrimaryInfecção pelo Zika virus / diagnósticopt_BR
dc.subject.decsPrimaryInterações Hospedeiro-Parasita / imunologiapt_BR
dc.subject.decsPrimaryMutagênese / imunologiapt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Microbiology & Immunology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA / University of Texas Medical Branch. Department of Microbiology & Immunology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA / Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA / Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Microbiology & Immunology. Galveston, TX, USA.pt_BR
dc.creator.affilliationMinistério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil / Pará State University. Department of Pathology. Belém, PA, Brazil.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Microbiology & Immunology. Galveston, TX, USA / University of Texas Medical Branch. Institute for Human Infections & Immunity. Galveston, TX, USA / University of Texas Medical Branch. Institute for Translational Science. Galveston, TX, USA / University of Texas Medical Branch. Sealy Center for Vaccine Development. Galveston, TX, USA / University of Texas Medical Branch. Sealy Center for Structural Biology & Molecular Biophysics. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Microbiology & Immunology. Galveston, TX, USA / University of Texas Medical Branch. Sealy Center for Vaccine Development. Galveston, TX, USA / University of Texas Medical Branch. Department of Pathology. Galveston, TX, USA.pt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Microbiology & Immunology. Galveston, TX, USA / University of Texas Medical Branch. Institute for Human Infections & Immunity. Galveston, TX, USApt_BR
dc.creator.affilliationUniversity of Texas Medical Branch. Department of Biochemistry & Molecular Biology. Galveston, TX, USA / University of Texas Medical Branch. Institute for Human Infections & Immunity. Galveston, TX, USA / University of Texas Medical Branch. Institute for Translational Science. Galveston, TX, USA / University of Texas Medical Branch. Sealy Center for Vaccine Development. Galveston, TX, USA / University of Texas Medical Branch. Sealy Center for Structural Biology & Molecular Biophysics. Galveston, TX, USA / University of Texas Medical Branch. Department of Phamarcology & Toxicology. Galveston, TX, USA.pt_BR
dc.identifier.doi10.1038/s41467-017-02816-2-


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