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 e Antigen Inhibits NF-kappaB Activity by Interrupting K63-Linked Ubiquitination of NEMO.
Abstract: It is reported that the hepatitis B e antigen (HBeAg) can interfere with NF-kappaB activity, which then leads to high viral loads, while HBV with the G1896A mutation remains infectious without the production of HBeAg but can induce more severe proinflammatory response and liver damage.
An Association Between Core Mutations in Hepatitis B Virus Genotype F1b and Hepatocellular Carcinoma in Alaskan Native People.
Abstract: In the HCC patients, T1938C and A2051C mutations in the core region had accumulated significantly with A1762T/G1764A mutations in the basal core promoter (BCP) region and G1896A mutation in the precore (PC) region.
Human hepatocytes apoptosis induced by replication of hepatitis B virus subgenotypes F1b and F4: Role of basal core promoter and preCore mutations.
Abstract: The BCPdm (A1762T/G1764A) and preCore (G1896A) mutants induced higher levels of apoptosis than the wt virus.
The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study.
PMID: 29628773
2018
Cancer management and research
Method: According to the sequencing outcome, HBV genotype and mutations (including A1752T/G, T1753C, G1757A, A1762T/G1764A, C1766T, T1768A, A1775G, C1799G, A1846T, T1858C, G1896A, G1898A, G1899A, and Pre S deletion) were confirmed by the BLAST analysis (http://blast.ncbi.nlm.nih.gov/Blast.cgi).
Result: According to different mutation regions, A1752T/G, T1753C,
Analysis of HBV basal core promoter/precore gene variability in patients with HBV drug resistance and HIV co-infection in Northwest Ethiopia.
Abstract: However, HBV mono-infected blood donors and CLD patients who had no any drug resistance gene variants developed comparable G1862T (60.6% vs. 65.1%) and G1896A (24.2% vs. 11.6%) PC gene mutations.
Abstract: RESULTS: Among the major mutant variants detected, double BCP mutations (A1762T/G1764A) (25.9%), Kozak sequences mutations (nt1809-1812) (51.7%) and the classical PC mutations such as A1814C/C1816T (15.4%), G1896A (25.2%) and G1862T (44.8%) were predominant mutant variants.
Table: G1896A
Figure: Prevalence comparison of th
A new hepatitis B virus e antigen-negative strain gene used as a reference sequence in an animal model.
PMID: 29339154
2018
Biochemical and biophysical research communications
Abstract: The G1896A variant resulted in a premature stop codon and abolished HBeAg expression.
Abstract: The main four point variants including A1762T, G1764A, G1896A, and G1899A were detected in the full-length genome.
Abstract: The strain will increase viral replication and infection for mutations A1762T and G1764A in the basal core promoter region, and mutations G1896A and G1899A in the pre-core region.
Clinical implication and viral mutation in basal core promoter/pre-core of hepatitis B virus C/D recombinant.
Abstract: The clonal frequencies of A1762T, G1764A, G1896A and A1846T were lower in patients with C/D than C2.
Abstract: but a lower frequency of G1896A stop mutation (33.6 vs. 76.5%, p < 0.001) was observed in patients with the C/D recombinant than in patients with genotype C2.
Virological and Clinical Characteristics of Hepatitis B Virus Genotype A.
Abstract: Regarding virological factors, the G1896A precore mutation is rarely observed in genotype A as it would disrupt an essential stem-loop structure in the epsilon signal essential for pregenomic RNA packaging.
The Correlation Between Hepatitis B Virus Precore/Core Mutations and the Progression of Severe Liver Disease.
PMID: 30406036
2018
Frontiers in cellular and infection microbiology
Introduction: One of the most common precore mutations reported thus far is a G1896A, which prevents HBeAg production through the replacement of a tryptophan residue at amino acid position 28 with a premature stop codon (Tong et al.,).
Introduction: Similarly, the role of the precore mutation G1896A and the basal core promoter
Discussion: One of the most common precore mutations, detected in more than 50% of individuals with chronic hepatitis B in Asia and the Mediterranean area, is a G to A substitution at nucleotide 1896, resulting in a tryptophan to stop codon substitution at codon 28 (Tong et al.,).