HBV Mutation Detail Information

Virus Mutation HBV Mutation G1862T


Basic Characteristics of Mutations
Mutation Site G1862T
Mutation Site Sentence We found point mutations upstream of the precore ATG codon of genotype Aa suppressed HBeAg expression, while the G1862T mutation in the precore region greatly impaired viral replication.
Mutation Level Nucleotide level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region PreC
Standardized Encoding Gene C  
Genotype/Subtype A
Viral Reference -
Functional Impact and Mechanisms
Disease Hepatitis B Virus Infection    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 16461214
Title Mechanism of HBV genome variability and replication of HBV mutants
Author Tong S
Journal Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
Journal Info 2005 Dec;34 Suppl 1:S134-8
Abstract Naturally occurring mutations in the H13V genome have been extensively documented, yet the biological consequences of even the dominant mutations have not been well characterized. In a recent study of HBeAg-positive French patients infected with genotype A, we obtained full-length clones with high or low replication capacities in the transfected human hepatoma cells. Surprisingly, high replicating clones were all derived from low viremia samples, and harbored core promoter mutations. The highest replicating clones all contained point mutations in addition to those at 1762/1764, and site-directed mutagenesis confirmed their role in further enhancing genome replication and suppressing HBeAg expression. Several core promoter mutants were defective in virion secretion, and mapping experiments revealed three missense mutations in the small envelope protein to be responsible: I110M, G119E, and R169P The effect of I110M and G119E mutations can be relieved by another point mutation that creates a novel N-linked glycosylation site. Finally, the African/Asian subgroup of genotype A (genotype Aa) contains unique mutations and is associated with low viremia titers as well as low HBeAg prevalence. We found point mutations upstream of the precore ATG codon of genotype Aa suppressed HBeAg expression, while the G1862T mutation in the precore region greatly impaired viral replication. Thus, molecular characterization can shed light on viral properties associated with clinical infection.
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.