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

• Main 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
• Other Authors: DUKE-NUS MEDICAL SCHOOL
• Format: Article
• Published: Nature Publishing Group 2020
• Subjects: 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; phylogeny; virology; Zika virus; Evolution, Molecular; Humans; Immune Evasion; Interferons; Mutation; Phylogeny; Protein-Serine-Threonine Kinases; Viral Nonstructural Proteins; Zika Virus; Zika Virus Infection
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/178458
• Institution: National University of Singapore

10.1038/s41467-017-02816-2