HBV Mutation Detail Information

Virus Mutation HBV Mutation K130M


Basic Characteristics of Mutations
Mutation Site K130M
Mutation Site Sentence Due to a compact viral genome organization, BCP1 and BCP2 mutations result in amino acids changes in the overlapping X gene: K130M/V131I and F132Y, respectively.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region X
Standardized Encoding Gene X  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Hepatitis B, Chronic    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 19439550
Title Genetic dissection of naturally occurring basal core promoter mutations of hepatitis B virus reveals a silent phenotype in the overlapping X gene
Author Hussain Z,Jung HS,Ryu DK,Ryu WS
Journal The Journal of general virology
Journal Info 2009 Sep;90(Pt 9):2272-81
Abstract During chronic hepatitis B virus (HBV) infection, double substitution mutations in the basal core promoter (BCP) region frequently emerge that include A1762T/G1764A and the neighbouring C1766T/T1768A mutations, here termed BCP1 and BCP2, respectively. Due to a compact viral genome organization, BCP1 and BCP2 mutations result in amino acids changes in the overlapping X gene: K130M/V131I and F132Y, respectively. It has been shown that both BCP mutations lead to a modest increase in viral genome replication. However, the question of whether the alteration that occurs in the overlapping X gene might contribute to the increased viral genome replication has not been properly addressed. This study genetically separated the core promoter from the overlapping X gene using 1.3mer overlength HBV constructs and examined the impact of the X gene mutations on viral genome replication in HepG2 cells. Each BCP mutation resulted in modestly enhanced viral genome replication that occurred via augmented viral transcription. Therefore, it was concluded that these BCP mutations do not affect expression of the overlapping X gene or impair its stimulatory effect on viral genome replication.
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.