HBV Mutation Detail Information

Virus Mutation HBV Mutation L21W


Basic Characteristics of Mutations
Mutation Site L21W
Mutation Site Sentence The results showed SFCs per 106 PBMCs were 30.4 ± 4.3 (95% CI 18.4 to 50.4) for the wild type, 16.7 ± 5.5 (9.3–30.0) for R24K, 17.7 ± 4.2 (10.9–29.0) for L21W, 12.5 ± 7.1 (6.4–24.5) for L21S/R24K, and 16.7 ± 5.6 (9.3–30.1) for L21S/R24K/Q30L, indicating that IFN-γ-secreting cells were lower towards variants in this region, particularly for R24K and L21S/R24K variants (paired t-test, p < 0.01)
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region S
Standardized Encoding Gene S  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease -
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location China
Literature Information
PMID 30771531
Title Diverse immune responses to HBV surface epitope variants after vaccine booster in adolescents immunized in infancy
Author Lai MW,Liang KH,Yeh CT
Journal Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases
Journal Info 2019 Sep;25(9):1140-1146
Abstract OBJECTIVES: We aimed to investigate immunity against hepatitis B surface antigen (HBsAg) mutants before and after boosters in adolescents who had lost antibodies against HBsAg (anti-HBs) despite neonatal vaccination. METHODS: We recruited 142 participants from 15 to 21 years old who had received complete vaccination in infancy but became anti-HBs-negative. Cellular immunity to HBsAg and T-cell epitope variants was assessed before and after boosters. Antibody affinity to variants was assessed after boosters. RESULTS: After one dose of booster, 12 out of 140 (8.6%) participants remained anti-HBs-negative. Anti-HBs titres were higher in those participants <17 (geometric mean, 337.9 +/- 10.9 vs. 157.4 +/- 16.6 mIU/mL, p = 0.012). Before the booster, HBsAg-specific cell proliferation was present in 58 out of 64 (90.6%) participants. The proliferation response rates to T-cell epitopes were 37.8% and 72.6% (p < 0.001) before and after the booster, respectively. The stimulation index improved from 1.25 +/- 1.70 to 2.53 +/- 2.32 (p < 0.001) for various T-cell epitopes. HBsAg-specific interleukin (IL)-5- and interferon (IFN)-gamma-secreting T-cells were enhanced (45 +/- 10 and 50 +/- 4 to 420 +/- 328 and 355 +/- 424 spot-forming cells/10(6) cells, respectively, p < 0.001). IFN-gamma-secreting T cells to epitope 16-33 containing R24K and the antibody affinity to sG145R were still significantly lower than to the wild type. CONCLUSIONS: In immunized adolescents who lost anti-HBs, around 10% also lost immune memory. Cellular immunity to some T-cell epitope variants improved after the booster. Antibody affinity to sG145R and the IFN-gamma-secreting cell response to some epitope 16-33 variants were still impaired even after booster administration.
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.