HBV Mutation Detail Information

Virus Mutation HBV Mutation V124M


Basic Characteristics of Mutations
Mutation Site V124M
Mutation Site Sentence Associated mutations were V124A;V124M;V124G;and V124E for V124;and T109S;T109I;T109M;T109C;and T109N for T109.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region C
Standardized Encoding Gene C  
Genotype/Subtype C
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 28401569
Title Influences on viral replication and sensitivity to GLS4, a HAP compound, of naturally occurring T109/V124 mutations in hepatitis B virus core protein
Author Wang J,Zhang H,Zhang Y,Jiang D,Li J,Goldmann S,Ren Q,Fei R,Wang X,Wei L
Journal Journal of medical virology
Journal Info 2017 Oct;89(10):1804-1810
Abstract Heteroaryldihydropyrimidine (HAP) compounds inhibit HBV replication by binding to a hydrophobic pocket at the interface between hepatitis B virus core protein (HBcAg) dimer, which interrupts capsid assembly by changing the kinetics and thermodynamics during this process. Structure biological studies have identified several amino acids in HBcAg crucial for compound binding. Here, we investigated the polymorphisms of T109 and V124 amino acids in HBV sequences submitted to GenBank database. Naturally occurring T109 and V124 and/or possible compensatory mutations in neighbored amino acids were introduced into HBV-expressing plasmids. Viral replication competence and sensitivity to GLS4, a HAP compound, were evaluated using transient transfection and in vitro infection cell models. All tested mutations in these amino acids led to decreasing viral DNA replication at different levels. Specially, T109N and all V124 mutants caused severe deficiencies in viral plus-strand DNA synthesis. T109I single mutation and all T109S/M/C/N mutations impaired HBeAg secretion. T109I showed modestly decreased sensitivities with IC50 3.3- to 6.8-folds higher than wild-type virus. In vitro infection assay showed T109N and all V124 mutants failed to synthesize cccDNA and following viral proteins. The other mutants, however, produced functional cccDNA pools as wild-type virus did. Taken together, we profiled the competences of viral replication and sensitivities to capsid inhibitor of naturally existing mutations in T109 and V124. This will help to understand the possible antiviral resistance issues in future clinical applications of capsid inhibitors.
Sequence Data 195957411;827344096;57835641;830677494;149211556;283466975;255653405;196051077;152963716;149211686;734652228;26665361;756447643;756447602;213495371;341830431;281190860;226876887;916337968;377692491;340748669;304273664;261288602;93004228;93004223;93004218;93004188;161788772;164654691;21280291;21280283;21280267;560087;560082;675274487;377814170;377814170;751242016;197292967;197292963;440235387;377692624;340748465;340748207;341830730;341830573;341830565;289598431;281191009;310914309;310914278;304273711;304273704;261288526;261288427;226876950;227336041;227335955;171345909;251822169;198278259;161788777;149211567;116812281;341830714;281191040;161788767;289598205
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.