JEV Mutation Detail Information

Virus Mutation JEV Mutation E138K


Lys mutation at residue 138 of the envelope protein (E-E138K) rendered the mutated RP-9 sensitive to the antiviral effect of IFN-alpha. --> Lys mutation at residue 138 of the envelope protein (E-E138K) rendered the mutated RP-9 sensitive to the antiviral effect of IFN-alpha. In A549 and Vero cells, the induction of three well-known ISGs, Stat-1, PKR, and IRF- 9, was observed in the mock- and RP-2ms-infected cells but not in the RP-9-infected cells (Fig. 4). -->
Basic Characteristics of Mutations
Mutation Site E138K
Mutation Site Sentence Thus, the E-E138K mutation of JEV appears to affect the viral growth properties, leading to a reduced efficiency in blocking IFN signaling, which then results in an attenuated phenotype in inoculated animals.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region E
Standardized Encoding Gene envelope
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Cell line    
Immune -
Target Gene IFNA1    STAT1    EIF2AK2    IRF9   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 19366580
Title A Japanese encephalitis virus vaccine candidate strain is attenuated by decreasing its interferon antagonistic ability
Author Liang JJ,Liao CL,Liao JT,Lee YL,Lin YL
Journal Vaccine
Journal Info 2009 May 11;27(21):2746-54
Abstract Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute encephalitis with high mortality in humans. To understand the virus-host interactions that influence JEV virulence, we determined the lethality of a neurovirulent (RP-9) and an attenuated (RP-2ms) variant of JEV in several immunodeficient mice strains. The attenuated phenotype of RP-2ms was completely lost in Stat-1-deficient mice, but its virulence was only slightly increased in mice lacking the components of adaptive immunity, suggesting an important role of the interferon (IFN) system in controlling JEV infection. Cell-based assays demonstrated that RP-2ms is more sensitive to IFN-alpha treatment; however, the NS5 protein of RP-2ms was still a potent antagonist of IFN, like RP-9 NS5. Using a recombinant infectious clone of RP-9, we found that a single Glu-->Lys mutation at residue 138 of the envelope protein (E-E138K) rendered the mutated RP-9 sensitive to the antiviral effect of IFN-alpha. Furthermore, IFN signaling was blocked earlier in the RP-9-infected cells relative to that in cells infected with RP-2ms or recombinant RP-9 bearing the E-E138K mutation. Thus, the E-E138K mutation of JEV appears to affect the viral growth properties, leading to a reduced efficiency in blocking IFN signaling, which then results in an attenuated phenotype in inoculated animals.
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.