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.
PMID: 18675784
2008
Biochemical and biophysical research communications
Abstract: A1762T and G1764A mutations in the basal core promoter are often present in HBV patients but seldom in asymptomatic carriers, and are highly correlated with the increased risk of HBV-associated hepatocellular carcinoma (HCC).
Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma.
PMID: 18695135
2008
Journal of the National Cancer Institute
Abstract: Among participants with a baseline HBV DNA level of at least 10(4) copies/mL, HCC incidence per 100 000 person-years was higher for those with the precore G1896 (wild-type) variant than for those with the G1896A variant (955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9]) and for those with the BCP A1762T/G1764A double mutant than for those with BCP A1762/G1764 (wild-type) variant (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% CI = 255.1 to 490.4]).
Abstract: Participants who had a baseline serum HBV DNA level greater than 10(4) copies/mL (n = 1526) were tested for the precore G1896A and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants.
PMID: 18844615
2008
The American journal of gastroenterology
Introduction: The common precore mutation (G1896A), mutations in enhancer II (C1653T) and the basal core promoter (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC.
Result: Almost all mutations at nt 1653 and nt 1753 are co-incident with the A1762T, G1764A mutations.
Result: Of the 2998 recruited initially, 740 were excluded: 638 because the BCP sequences could not be determined at baselin
Core promoter mutant HBV non-responding to adefovir after viral breakthrough on lamivudine: rapid virologic response to tenofovir plus lamivudine in a cirrhotic patient.
PMID: 19008175
2008
European journal of medical research
Abstract: Because of unchanged VL sequence analysis was performed three months later, which showed the mutation (rtS219A) and the concomitant mutation (sS210R) and 2 mutations in core promoter region (A1762T), (G1764A).
Genotype and variations in core promoter and pre-core regions are related to progression of disease in HBV-infected patients from Northern Vietnam.
PMID: 17203204
2007
International journal of molecular medicine
Abstract: The presence of the mutation A1762T/G1764A correlated with disease progression.
Abstract: The triple mutation T1753C/A1762T/ G1764A was quite common and was more prevalent in LC and HCC than in CH and ASC.
Clinical and virological characteristics of hepatitis B virus subgenotypes Ba, C1, and C2 in China.
PMID: 17376881
2007
Journal of clinical microbiology
Abstract: In contrast, HBV Ba had the highest frequency of 1896A but the lowest of A1762T G1764A, and HBV C2 had intermediate frequencies of these mutations.
Abstract: Multivariate analyses showed that the 1653T, 1753V, and A1762T G1764A mutations and patient age significantly increased the risk of HCC development.
Abstract: Therefore, genotyping and detecting the 1653T and 1753V mutations, in addition to the A1762T G1764A double mutation, might have important clinical implications as predictive risk factors for hepatocarcinogenesis.
Abstract: Virologically, HBV C1 had the strongest association with the A1762T G1764A<
Initial load of hepatitis B virus (HBV), its changing profile, and precore/core promoter mutations correlate with the severity and outcome of acute HBV infection.
Abstract: In univariate analysis, seronegativity for hepatitis B envelope antigen (HBeAg) and mutations in both the precore (G1896A and/or G1899A) and core promoter (T1753A/C and/or T1754C/G and/or A1762T/G1764A) were associated with FH (odds ratio [OR], 5.60; P=0.0269 and OR, 52.0; P=0.0006; respectively).
A weak association between occult HBV infection and non-B non-C hepatocellular carcinoma in Japan.
Abstract: In the NBNC-HCC group, the determined nucleotide sequences of the enhancer II/core promoter/precore/core region did not contain any HCC-associated mutations, whereas 25 of 30 patients in the HBV-HCC group carried strains with C1653T, T1753V, and/or A1762T/G1764A mutations.
Presence of hepatitis B virus core promoter mutations pre-seroconversion predict persistent viral replication after HBeAg loss.
Abstract: We found that the hot spot mutations (A1762T/G1764A) only mildly reduced HBeAg expression and enhanced genome replication, while incorporation of additional core promoter mutations intensified both phenotypes.
HBV mutation literature information.
PMID: 
2008
Biochemical and biophysical research communications
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