Transcriptome analysis of hepatoma cells transfected with Basal Core Promoter (BCP) and Pre-Core (PC) mutant hepatitis B virus full genome construct.
PMID: 33595430
2021
The Journal of general virology
Abstract: Infections with Basal Core Promoter (BCP) (A1762T/G1764A) and Pre-Core (PC) (G1896A) hepatitis B virus HBeAg mutants are associated with severe liver injury.
The Occurrence of rtA194T Mutant After Long-Term Lamivudine Monotherapy Remains Sensitive to Tenofovir Disoproxil Fumarate: A Case Report.
Discussion: However, G1896A or A1762T/G1764A mutations were not found in this patient with genotype C HBV by DNA sequencing, while A1727T, C1730G and C1799G mutations were found in BCP region, which were reported to be associated significantly with cirrhosis.
Hepatitis B virus genome diversity in adolescents: Tenofovir disoproxil fumarate treatment effect and HBeAg serocon version.
Abstract: The basal core promoter (BCP) variants, A1762T and G1764A, and the pC variant, G1896A, were most often enriched at or after seroconversion.
Increased hepatitis B virus quasispecies diversity is correlated with liver fibrosis progression.
PMID: 34029727
2021
Infection, genetics and evolution
Abstract: Specific mutations, such as A1762T, G1764A and G1896A, in the BCP/PC region were more common in patients with advanced liver disease and formed the majority of the viral quasispecies pool in patients with LC and HCC.
Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants.
Abstract: HBV variants, particularly the G1896A pre-core (PC) and A1762T/G1764A basal core promoter (BCP) mutations, are established risk factors for cirrhosis and HCC, but the molecular biological basis is unclear.
Abstract: RESULTS: HBeAg expression was reduced in PC and BCP variants, and higher supernatant HBV DNA and HBV RNA levels were found with A1762T/G1764A vs. G1896A mutant (p_< 0.05).
Discussion: However, these in vivo findings are in contrast with our in vitro results in which secreted HBV
Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection.
Abstract: Through application of deep whole-genome sequencing we typed the isolate as genotype-D1, and identified several minority variants including G1764A and G1986A substitutions in the pre-core promoter and pre-core regions, which support CHB-AR rather than AHB.
Conclusion: The most prevalent minority variant mutations in our HBV sequences were G1896A, G1899A and G1764A (precore/core and basal core promotor sequences respectively) ( Table 1).
Table: G1764A
Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region.
Abstract: HCC-associated mutations were detected in 33.7% of the sequences, with significantly higher frequency of C1653T, T1753V and A1762T/G1764A in genotype G than C (P < 0.001).
Result: C1653T, T1753V and A1762T/G1764A were highly frequent in genotype G (95, 95, and 97.5%, respectively), followed by genotype C (12, 18.1, and 46.1%, respectively), while Pre-S deletions prevailed in genotype C (3.3%) (Table 1).
Result: Significant differences in A1762T/G1764A rates were found within genotypes B, C, D, and F, with subgenotypes B
Viral hepatitis B and C in HIV-exposed South African infants.
5Result: The ""Week 0"" Cape Town sample showed a similar serological profile to the ""Week 48"" sample from the same child and also had the double A1762T/G1764A BCP mutation."
Abstract: The Result: Both sequences harboured the double A1762T/G1764A BCP mutation.
Result: Sequence analysis revealed the M204I mutation in the reverse transcriptase domain of the polymerase gene in the Durban sample while the Cape Town sample harboured the double A1762T/G1764A BCP mutation in the core gene.
Optimization of the algorithm diagnosis chronic hepatitis B markers in patients with newly diagnosed HIV infection.
Abstract: When analyzing the basal nucleus promoter, Precore and Core regions, 22.2% of patients with the double mutation A1762T / G1764A, 25% with the mutation G1896A were identified.
Quadruple mutation GCAC1809-1812TTCT acts as a biomarker in healthy European HBV carriers.
Abstract: Calculation of the pgRNA secondary structure suggests a destabilization of the pgRNA structure by A1762T/G1764A that was compensated by GCAC1809-1812TTCT.
Abstract: GCAC1809-1812TTCT was strongly associated with coexistence of basal core promoter (BCP) double mutation A1762T/G1764A and lower HBV DNA levels.
Result: After the implementation of GCAC1809-1812TTCT in addition to A1762T/G1764A (Figure 5C), the RNA secondary structure was stabilized by a hairpin structure and the MFE decreased approximately to the WT level (-69.1 kcal/mol; GC content of 46%).
Result: Although this mutation was found in 66% (226 of 340) of the samples with A1762T/<
HBV mutation literature information.
PMID: 
2021
The Journal of general virology
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