Abstract: Our results show that for the subgenotype (sgt) D1, which has an 8-nucleotide deletion (sgtD1del) and exhibits lower fitness, the levels of extracellular DNA and intracellular replicative intermediates were much lower than with sgtD1wt or sgtD1mut (G1896A), which had higher fitness.
Hepatitis B virus in Mar del Plata, Argentina: Genomic characterization and evolutionary analysis of subgenotype F1b.
Abstract: A unique D3 presented the G1896A substitution at the preC (HBeAg negative phenotype).
Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients.
Method: Furthermore, mutants C18T, G82A, A115C, G120A, A138G, and C189A in SPII were cloned into a plasmid pBlueBac4.5 1.2/PC (p1.2/PC) respectively, which contained a 1.2-fold length HBV genome of genotype C2 with a G1896A mutation in the preC region.
Molecular and serological characterization of hepatitis B vaccine breakthrough infections in serial samples from two plasma donors.
Discussion: Neither the precore stop codon mutation G1896A which abolishes HBeAg production or the basal core promoter mutations which cause reduced HBeAg production were found in any samples from either panel.
Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients.
PMID: 31308922
2019
Mediterranean journal of hematology and infectious diseases
Abstract: Conclusions: Our results showed common mutations within HBsAg, occurring in immune epitopes, a high rate of G1896A mutations in the PC region, and a negative correlation between the emergence of A1762T/G1764A mutation and the G1764T/C1766G
Introduction: The most common mutations involve G1896A in the PC region and the simultaneous presence of G1764A/A1762T in the BCP region, which results to the premature termination of HBeAg expression and decreased level of HBeAg, respectively.
Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B.
Abstract: No significant difference between groups was found regarding C1653T and G1896A mutants.
Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations.
PMID: 31341412
2019
International journal of medical sciences
Introduction: The precore mutation (G1896A), mutations in enhancer II (C1653T) and the BCP (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC.
Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients.
Result: Although G1896A frequently disrupts the production of HBeAg via the introduction of a premature stop codon, other mutations are likely to achieve a similar clinical effect via different molecular means.
Result: Aside from C1817T and A1838G variants, it is worth mentioning that C1653T, G1896A, and G1899A displayed the next most significant association with viral load in the discovery patient cohort (LRT p = 6 x 10-8, p = 6.7 x 10-8, and p = 2.3 x 10-7, respectively).
Result: Aside from its previously mentioned role in the epsilon region of the pgRNA, G1896A introduces a stop codon in the precore region abolishing HBeAg
The Effect of the Hepatitis B Virus Surface Protein Truncated sC69( *) Mutation on Viral Infectivity and the Host Innate Immune Response.
Method: We cloned the sC69* mutant into plasmid pBB4.5 1.2/PC, which contained a 1.2-fold length HBV genome of genotype C with a G1896A mutation in the precore region.
Analysis of hepatitis B virus genotype and gene mutation in patients with advanced liver disease in East Kalimantan, Indonesia.
Abstract: The C1505A mutation in X region, T1753V and A1762T/G1764A mutations in the basal core promoter region and C1858T in precore (PC) region were frequent and only detected in patients with ALD (28.9, 40, 73.5 and 17.6%, respectively), whereas the G1896A mutation in the PC region was frequently detected in HBV carriers.
HBV mutation literature information.
PMID: 
2019
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