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
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 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.
Abstract: The frequencies of these HBeAg seroconversion-related mutations were significantly lower in HBeAg-negative children with CHB than in HBeAg-negative adults with CHB, especially for the mutation G1896A (41.1% vs 91.7%, P<0.001), and the average number of BCP/precore region mutations in samples from HBeAg-negative child patients was also obviously lower than in HBeAg-negative adult patients(3.62+-3.03 vs 4.89+-2.09, P<0.001), suggesting less impact of mutations in the BCP/precore region on HBeAg se
Hepatitis B virus genotype distribution and genotype-specific BCP/preCore substitutions in acute and chronic infections in Argentina.
Discussion: Furthermore, despite the fact that all subgenotypes D have T1858, only subgenotypes D1 and D7 have a tendency to mutate G1896A.
Discussion: Given the fact that pC region overlaps the encapsidation signal, which is essential for efficient replication, those genotypes with T1858 would tend to mutate G1896A in order to increase stability of the stem loop in the encapsidation signal structure.
Discussion: In summary, those genotypes carrying 1858C seem to prevent G1896A mutation; however, T1858 polymorphism seems to be necessary but not sufficient to promote G1896A substitution.
Discussion: On the other hand, the high prevalence of mutations other than G1896A in the preCore region in subgenotype A2 indicates
Correlation Between Hepatitis B G1896A Precore Mutations and HBeAg in Chronic HBV Patients.
PMID: 25825644
2015
Jundishapur journal of microbiology
Introduction: In this study, the G1896A precore mutation and its effect on HBeAg detection were investigated in chronic HBV patients, using polymerase chain reaction (PCR) and subsequent sequencing method, rather than the restriction fragment length polymorphism (RFLP), because of improving the sensitivity of the detection.
Introduction: The most common of these mutations is a guanine (G) to adenine (A) substitution at nucleotide1896, which prevents the production of HBeAg by introducing a premature stop codon into the open reading frame (ORF) of the PC.
Introduction: The predominant mutation involves a GtoA change at nucleotide1896 (A1896), which creates a premature stop
New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing.
Result: As compared with non-ACLF cases, T216C, G285A, A1846T/G, G1896A, C1913A/G, A2159G/C, A2189T/C in genotype B and G285A, A1846T/G, G1896A, C1913A/G and A2159G/C in genotype C were significantly associated with an increased risk of ACLF(see Table 5).
Result: In ACLF group, the mutations at seven sites (T216C, G285A
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).
G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic 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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