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.
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
Discussion: Some studies indicated that the A1
Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients.
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double mutation were observed in early seroconversion processes in a longitudinal study of infants (our own unpublished data), which also supports the idea that HBeAg seroconversion does not solely rely on BCP/precore mutations.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.
Abstract: In anti-HBe positive chronic infections, sgF1b was more prone to have A1762T/G1764A mutation than sgA2, sgF4 and gD (75.0, 40.0, 33.3 and 31.8%, p<0.005), whereas in the pC region, gD and sgF4 were more likely to have G1896A than sgA2 and sgF1b (81.0, 72.7, 0.0 and 31.3%, p <0.001).
Abstract: The unexpected low frequency of the G1896A mutation in the sgF1b (despite carrying 1858T) prompted us to perform a further analysis in order to identify genotype-specific features that could justify the pattern mutations observed.
Result: In brief, those patients infected with sgF4 and gD mutated G1896A more frequently than A1762T/G1896A mutation in patients with different spectrum of hepatitis B.
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
Discussion: The clinical relevance of the G1896A PC mutation in chronic hepatitis B (CHB) is still poorly understood.
New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing.
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
Discussion: Also it was found that the frequencies
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.
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).
LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B.
Abstract: BACKGROUND: Precore stop codon (G1896A) mutation is one of the commonest mutations found in patients with chronic hepatitis B.
Abstract: CONCLUSIONS: Our data suggested an intermediate prevalence of G1896A mutation among Malaysian hepatitis B carriers.
Abstract: Clinical association revealed that subjects with G1896A mutations were mainly detected in asymptomatic chronic hepatitis B (58.3%) and liver cirrhosis (41.7%).
Abstract: No significant association was observed between G1896A mutation and HBeAg-negativity.
HBV mutation literature information.
PMID: 
2015
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