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.
Figure: Four patterns (preC-/CP-, preC+/CP-, preC-/CP+, and preC+/CP+) were defined based on the presence (+) or absence (-) of pre-C mutation G1896A and CP A1762T/G1764A double mutation.
Discussion: All these results led us to speculate that persistent HBV replication after HBeAg seroconversion occurs independently of G1896A
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.
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: 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.
Abstract: There is no statistically significant link between G1896A and genotypes.
Frequency and clinical significance of core promoter and precore region mutations in Tunisian patients infected chronically with hepatitis B.
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.
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 precore mRNA; the Kozak sequence mutants that affect HBeAg translation; precore start cod
[Analysis of the relationship between hepatitis B virus precore and basal core promoter mutations and acute-on-chronic liver failure].
Abstract: Single mutations (A1762T, G1764A, T1753V, G1896A, and G1899A) and combined mutations (A1762T + G1764A, G1896A + G1899A, T1753V+ A1762T + G1764A, G1896A + G1899A + A1762T + G1764A, and A1762T + G1764A + G1896A) were more frequently detected in HB-ACL
HBV Subgenotype C2 Infection, A1762T/G1764A Mutations May Contribute To Hepatocellular Carcinoma with Cirrhosis in Southeast China.
PMID: 23304671
2012
Iranian journal of public health
Introduction: HBV mutations were often observed in the pre-C and basal core promoter (BCP) regions, such as T1753C, A1762T, G1764A, G1862T, G1896A and G1899A nucleotide acid substitution.
Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence.
Introduction: Several epidemiological studies have shown that HBV genotype D was predominant in the Tunisian population, and frequencies of double mutation A1762T /G1764A in BCP region and common mutation G1896A in PC region of viral B genome were higher among asymptomatic chronic carriers.
Result: Of limited number of 1858C variant virus examined in this study, none of them was found to have 1896A mutation when mutant G1896A was associated with double mutation A1850T and C1858T.
Result: Only 20 isolates out of 34 HBeAg-negative cases were found to have G to A mutation at nt 1896.
HBV mutation literature information.
PMID: 
2012
PloS one
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