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 HBV mutation literature information.


  Clinical significance of hepatitis B virus precore and core promoter variants in Korean patients with chronic hepatitis B.
 PMID: 24406435       2015       Journal of clinical gastroenterology
Abstract: METHODS: We assessed serum HBeAg, HBV DNA levels, alanine transferase (ALT) levels, and progression of liver fibrosis in 226 Korean CHB patients, presumed to be infected with genotype C HBV, to analyze HBV variants in the preC region (G1896A) and CP regions (A1762T, G1764A).


  Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C.
 PMID: 25741368       2015       Hepatitis monthly
Table: G1896A


  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
Abstract: CONCLUSIONS: In this population with chronic HBeAg negative hepatitis B, an association was observed between the G1896A mutation in the Pre-core region of HBV and subsequent level of HBV DNA seven years later, which indicated that mutations in this region of HBV genome may contribute to disease progression in these patients and play an important role in HBV natural course of disease.
Introduction: In addition, clinical and mechanistic importance of pre-core mutations are unclear; especially G1896A, which results in a premature stop codon and termination of HBeAg translation, but does not seem to affect viral replication.
Table: G1896A


  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: Although the G1899A mutation only changes the glycine at codon 29 into aspartic acid and is always accompanied by the G1896A mutation, a previous study revealed that approximately 50% of the HBeAg negative variants contained this combined mutation.
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double mutation were observed in early seroconversion processes in a longitudinal study of infants (our own unpublished data), which also supports the idea that HBeAg seroconversion does not solely rely on BCP/precore mutations.
Discussion: In these six


  Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina.
 PMID: 25822666       2015       PloS one
Introduction: Based on the stability of the encapsidation signal (nt 1847-1907) it has been established that genotypes carrying 1858T (B, C2, C3, D, E, F1 and F4) favor the emergence and selection of G1896A, whereas the double mutation A1762T/G1764A in the BCP is more prone to occur in those genotypes carrying 1858C (A, C1, F2, F3 and H).
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 order to assess the role of 1727, 1740 and 1773


  Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients.
 PMID: 25825644       2015       Jundishapur journal of microbiology
Discussion: A higher rate (95.3%) of the G1896A mutation was also reported in the HBeAg-negative group.
Discussion: In agreement with our results, a study from Brazil showed that the G1896A PC mutation occurred in 36% of Brazilian patients with CHB, of which 58.6% were HBeAg-negative.
Discussion: The G1896A mutation in the PC region has been found to be the most


  New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing.
 PMID: 25849554       2015       PloS one
Abstract: Multivariate analysis showed that T216C, G1896A, C1913A/G and A2159G/C were independent risk factors for ACLF.
Abstract: The results of Illumina sequencing showed that the mutations at 7 sites (T216C, G285A, A1846T, G1896A, C1913A/G, A2159G, and A2189C) of 12 ACLF patients were significantly higher than those of 12 controls.
Table: G1896A


  Characterization of Full-Length Genomes of Hepatitis B Virus Quasispecies in Sera of Patients at Different Phases of Infection.
 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.


  Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis.
 PMID: 26063382       2015       Virology journal
Abstract: CONCLUSIONS: The HBV basal core promoter/pre-core mutations T1753V, A1762T, G1764A, C1766T, T1768A, A1846T, G1896A and G1899A, and an HBeAg-negative status correlate with an increased risk of HBV-ACLF.
Abstract: Several mutations were significantly correlated with ACLF: T1753V (1.889, 95 % confidence interval (CI) [1.357-2.631]), A1762T (2.696 [2.265-3.207]),  PMID: 26587212       2015       Jundishapur journal of microbiology
Result: Analysis of the pre-core/core regions showed nucleic acid replacement in position G1896A, which results in an unwanted stop codon ( Figure 4).



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