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 HBV mutation literature information.


  Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran.
 PMID: 25788956       2015       Hepatitis monthly
Discussion: In contrast to these findings, cross-sectional studies of HBV viral level and liver disease severity have generally suggested associations with A1762T/G1764A double mutation, although these studies were mostly conducted among participants with other HBV genotypes.
Discussion: Some studies indicated that the A1762T/G1764A mutation typically appears earlier than G1896A during the course of HBV infection.


  Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients.
 PMID: 25822176       2015       PloS one
Discussion: An A1762T/G1764A double mutation in the BCP/precore region would reduce the levels of HBeAg by inhibiting precore mRNA expression, leading to the transition from the immune tolerance to the immune reactive phase, followed by lower DNA viral loads and elevated ALT levels.
Discussion: Deletions in core regions instead of the G1896A and A1762T/G1764A double mutation were observed in early seroconversion processes in a longitudinal study of infants (our own unpublished data), which also supports the idea that HBeAg seroconversion does not solely rely on BCP


  Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina.
 PMID: 25822666       2015       PloS one
Result: In brief, those patients infected with sgF4 and gD mutated G1896A more frequently than A1762T/G1764A (p = 0.007 and p<0.001 respectively), whereas those patients carrying sgF1b and sgA2 had the opposite mutation pattern, showing higher rates of mutations in positions 1762 and 1764 than in 1896 (p = 0.013 and p = 0.010 respectively).
Result: In spite of the low prevalence of mutations in AHB infections (25.7%), those subgenotypes more frequently observed in this stage, sgA2 and sgF1b, had the double mutation A1762T/G1764A, while gD and sgF4 did not mutate these positions (Table 3).
Result: The double mutation A1762T/G1764A was more frequently found in sgF1b infections (75.


  Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma.
 PMID: 25881591       2015       Chinese medical journal
Introduction: We and others have reported that HBV mutations C1653T, T1753V, A1762T/G1764A, T1674C/G, and C1766T/T1768A in the enhancer II/basal core promoter (EnhII/BCP) region; G1899A, C2002T, A2159G, A2189C, and G2203A/T in the precore/core region; as well as T53C,  PMID: 25926495       2015       Journal of clinical microbiology
Abstract: A triple mutation (A1762T/G1764A/G1896A) was observed more frequently in genotype C than in genotype B.


  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: 26165271       2015       Molecular medicine reports
Abstract: The double nucleotide, A1762T and G1764A exchange (TA mutation), in the hepatitis B virus (HBV) genome basal core promoter (BCP) region is a common viral mutation in patients with chronic HBV infection.


  Distribution of hepatitis B virus genotype and cancer predicting precore and basal core promoter mutations.
 PMID: 26288490       2015       Medical journal, Armed Forces India
Abstract: The total Double mutations of BCP at A1762T/G1764A nucleotide positions, and PC mutation at G1896A nucleotide position were seen in 29.3% and 21.3%, respectively.
Abstract: Viral factors that may increase the risk for HCC development include HBV DNA level, genotypes, and naturally occurring mutations such as hepatitis B virus precore (PC) (G1896A) and basal core promoter (BCP) A1762T/G1764A double mutations.


  Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study.
 PMID: 26290395       2015       Cancer prevention research (Philadelphia, Pa.)
Abstract: In control patients carrying A1762T/G1764A, addition of C1653T and/or T1753V significantly increased HCC risk (HR, 1.57; P = 0.038); combo mutations with C1653T, T1753V, and A1762T/G1764A improved the validity of HCC prediction by age, male, and cirrhosis (P = 0.002).
Abstract: In summary, HBV mutation A1762T/G1764A, C1653T, and T1753V in combination improve  PMID: 26447624       2015       Zhonghua gan zang bing za zhi
Abstract: CONCLUSION: Incidence of the T1674C mutation in the X region and of the T1753C mutation and the A1762T/G1764A double mutation in the BCP region was higher for patients with HBV-related HCC; the T1753C mutation and the A1762T/G1764A double mutation may inhibit the formation of HBeAg.
Abstract: Prevalence of the T1753C mutation and the A1762T/G1764A double mutation in the BCP region was significantly higher in the  PMID: 26543337       2015       Chinese journal of cancer research
Abstract: CONCLUSIONS: This study demonstrated that PreS mutations, C1653T, T1753V, and A1762T/G1764A, were associated with an increased risk of HCC.
Abstract: For mutations in BCP, statistically significant pooled-RRs of HCC were obtained for T1753V (pooled-RR=2.09; 95% CI: 1.49-2.94) and A1762T/G1764A double mutations (pooled-RR=3.11; 95% CI: 2.08-4.64).



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