HBV Mutation Detail Information

Virus Mutation HBV Mutation W172L


Basic Characteristics of Mutations
Mutation Site W172L
Mutation Site Sentence One mutant resulted in a stop codon at HBsAg position 172 (rtA181T/sW172*), whereas the other mutant resulted in an amino acid change at HBsAg position 172 (rtA181T/sW172L). The rtA181T/sW172L + rtN236T and rtA181V + rtN236T double mutants were created by two rounds of mutagenesis.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region S
Standardized Encoding Gene S  
Genotype/Subtype D;B;C
Viral Reference -
Functional Impact and Mechanisms
Disease Hepatitis B Virus Infection    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment Abacavir(ADV)
Location US
Literature Information
PMID 24118725
Title HBV clinical isolates expressing adefovir resistance mutations show similar tenofovir susceptibilities across genotypes B, C and D
Author Liu Y,Miller MD,Kitrinos KM
Journal Liver international : official journal of the International Association for the Study of the Liver
Journal Info 2014 Aug;34(7):1025-32
Abstract BACKGROUND & AIMS: Hepatitis B virus (HBV) genotypes can influence clinical outcomes as well as response to antiviral therapy. This study evaluated the tenofovir (TFV) susceptibility of HBV genotype B, C and D clinical isolates with adefovir resistance-associated mutations (ADV-R). METHODS: Full-length HBV isolates from patients infected with genotype B, C and D virus had rtA181T, rtA181V, rtN236T, rtA181T+rtN236T and rtA181V+rtN236T mutations introduced by site-directed mutagenesis. Phenotypic analyses were performed in HepG2 cells and susceptibility to TFV and ADV were assessed. RESULTS: Clinical HBV isolates containing rtA181T, rtA181V or rtN236T as single mutants remained sensitive to TFV across genotypes B, C and D. Clinical isolates containing the rtA181T+rtN236T double mutant remained sensitive to TFV in genotype D but exhibited reduced susceptibility to TFV in genotypes B and C. Viruses containing the double mutant rtA181V+rtN236T in genotypes B and D exhibited reduced susceptibility to TFV with EC50 fold changes (FC) of 3.8 and 2.5, respectively, while genotype C viruses containing rtA181V+rtN236T either remained sensitive (FC=1.3) or exhibited reduced susceptibility to TFV (FC=2.9) depending on the isolate. All rtA181V+rtN236T isolates conferred reduced susceptibility to ADV (FC values 2.3-4.2). CONCLUSIONS: Genotype B, C and D isolates with single ADV resistance mutations remained fully sensitive to TFV, while the double mutants rtA181T+rtN236T and rtA181V+rtN236T exhibited either no change or low-level reduced susceptibility to TFV across genotypes. These results are consistent with the clinical efficacy observed with tenofovir disoproxil fumarate (TDF) treatment across all genotypes in vivo and the limited impact of ADV-R mutations on TDF therapy.
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.