Abstract: The precore mutation G1896A was identified in 35% of all specimens, and was more frequently observed in genotype B (41%) than genotype C (3%; p<0.0001).
Result: 35% of all specimens had the precore stop mutation G1896A which abrogates HBeAg production; however, this was detected in 41% of genotype B compared to only 3% of genotype C viruses (p<0.0001; Figure 4).
Result: Evaluation of fragments for which there was an available corresponding S gene sequence also identified a difference in mutational patterns at the subgenotype level: B2 viruses compared to B4 for both G1896A (20%, n = 1/5 vs 40.2%, n = 53/132) and A1762T/G1764A (40%, n = 2/5 vs 19.
Hepatitis B virus gene mutations in liver diseases: a report from New Delhi.
Introduction: Although the T1762/A1764 double mutation, commonly occurring in HBeAg-negative patients, was observed in vivo to suppress the production of preC mRNA independent of G1896A, recent in vitro research suggested other single site substitutions rather than these two which may be responsible for the reduction of HBeAg expression.Unknown mutation in this core promoter may impede the seroconversion of HBeAg during antiviral treatment.
Introduction: Studies have shown that G1896A is involved in HBeAg negativity by introducing a stop codon in the preC region.
Table: G1896A
Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression.
Introduction: G1896A mutation was seen at a higher frequency in genotype D strains, while A1762T/G1764A double mutation was observed predominantly in genotype A strains.
Introduction: Moreover, other studies reported no association between G1896A and clinical outcome.
Introduction: Our previous study focused only on pre-C G1896A and G1899A mutations by using selective oligonucleotide hybridization, and showed a predominance of these variants.
Introduction: The clinical significance of G1896A mutation is unclear, with reports of its association with severe forms of liver disease and others of its occurrence in a large number of patie
High prevalence of the B2+C2 subgenotype mixture in patients with chronic hepatitis B in Eastern China.
Abstract: A double mutation (G1896A) in the PC was significantly more common in subgenotype B2+C2 than in subgenotype B2+C1.
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.
Abstract: The A1762T/G1764A or G1896A mutations were detected in 125specimens (125/192, 65.10%), in which 77 (77/125, 61.60%) existed as subpopulations.
Abstract: The present study was aimed to obtain baseline information of basal core promoter A1762T/G1764A and precore G1896A mutations of hepatitis B virus (HBV) in 192 HBeAg-positive chronically-infected Chinese patients, who were potential candidates for antiviral treatment.
Hepatitis B virus basal core promoter mutations A1762T/G1764A are associated with genotype C and a low serum HBsAg level in chronically-infected HBeAg-positive Chinese patients.
Abstract: Mutations affecting HBeAg expression at the transcriptional (1762T1764A), translational (Kozak 1809-1812, initiation 1814-1816, G1896A with C1858T), or post translational levels (G1862T), were responsible for the high HBeAg-negativity observed.
Result: The classical G1896A mutation occurred in five isolates and in four cases it occurred together with C1858T.
Discussion: The HBeAg negativity found in 44/49 Shongwe participants (89,7%) could be accounted for by the following HBV mutations: the basic core promoter mutations A1762T/G1764A, which can down-regulate transcription of
[Analysis of the relationship between hepatitis B virus precore and basal core promoter mutations and acute-on-chronic liver failure].
HBV mutation literature information.
PMID: 
2012
Journal of medical virology
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