ZIKV Mutation Detail Information

Virus Mutation ZIKV Mutation V188A


Basic Characteristics of Mutations
Mutation Site V188A
Mutation Site Sentence In contrast, FSS13025 WT and PRVABC-59 V188A NS1 proteins were not able to antagonize IFN-β activation induced by MAVS, IKKε, TBK1, or IRF3/5D (Fig. 3c–f).
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region NS1
Standardized Encoding Gene NS1
Genotype/Subtype -
Viral Reference KU955593.1;KU501215;KU955591.1
Functional Impact and Mechanisms
Disease Cell line    
Immune Y
Target Gene IFNB1    IKBKE    TBK1    IRF3   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location Cambodia;Puerto Rico;Dakar
Literature Information
PMID 29379028
Title An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction
Author Xia H,Luo H,Shan C,Muruato AE,Nunes BTD,Medeiros DBA,Zou J,Xie X,Giraldo MI,Vasconcelos PFC,Weaver SC,Wang T,Rajsbaum R,Shi PY
Journal Nature communications
Journal Info 2018 Jan 29;9(1):414
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-beta 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-beta induction; reversing the mutation in an epidemic ZIKV strain invigorates the virus for interferon-beta induction; these mutational effects are lost in IRF3-knockout cells. Additionally, ZIKV NS2A, NS2B, NS4A, NS4B, and NS5 can also suppress interferon-beta 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.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.