CHIKV Mutation Detail Information

Virus Mutation CHIKV Mutation T376M


Basic Characteristics of Mutations
Mutation Site T376M
Mutation Site Sentence In addition to A226V mutation, the virus was having four unique amino acid substitutions, two from nonstructural (Nsp1: T128K and T376M) and two from structural proteins (Capsid: P23S and V27I) as compared to S-27 prototype Chikungunya virus strain.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region nsP1
Standardized Encoding Gene nsP1
Genotype/Subtype -
Viral Reference EU372006
Functional Impact and Mechanisms
Disease Chikungunya Fever    
Immune -
Target Gene TLR3    TLR7    TLR8    TLR9    TRAF6    TICAM1    IRF1    IRF3    IRF7    CCL2    CXCL10    IL6    ISG15    MX2    IFNB1    OAS3   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 24905288
Title TLR3 mediated innate immune response in mice brain following infection with Chikungunya virus
Author Priya R,Patro IK,Parida MM
Journal Virus research
Journal Info 2014 Aug 30;189:194-205
Abstract Chikungunya virus (CHIKV) has received global attention due to the series of large-scale outbreaks in different parts of the world. Many unusual clinical severities including neurological complications and death were reported in recent outbreaks. The mechanism underlying the host immune response to CHIKV in the brain is poorly characterized. In this study, the neuropathogenesis of CHIKV with E1:A226V mutation was elucidated in 1 week old BALB/c mice. The virus was found to replicate in mice brain with peak titer of 10(4) on 6th day post infection. Immunohistochemical analysis revealed preferential virus localization in neuronal cells of cerebellum. The expression profiling of TLR, antiviral genes and cytokines in mice brain revealed significant up regulation of TLR3, TRAF-6, TICAM-1, MCP-1, CXCL-10, IL-6, IL-4, ISG-15, MX-2, IFN-beta, OAS-3 genes that ultimately resulted in virus clearance from brain by day 9-10 suggesting activation of innate immune pathway. Further the effect of poly I: C (Polyinosinic: Polycytidylic acid), a TLR-3 agonist and potent IFN inducer on CHIKV neuropathogenesis was studied. Pretreatment of mice with Poly I: C caused reduction of CHIKV titer in brain and offered 100% protection of animals. The protection was mediated by an increased induction of TLR3, IFN-beta and antiviral genes in mice brain. Our result demonstrates that pre immune stimulation of animals by Poly I: C is effective inhibitor of CHIKV replication and might be a promising prevention agent against this virus.
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.