LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B.
PMID: 30505167
2018
Saudi journal of biological sciences
Abstract: It is of utmost importance to screen the G1896A precore mutation.
Abstract: LCR can be a suitable tool for screening of G1896A mutations.
Abstract: Patients were screened for the presence or absence of precore G1896A mutation by PCR-LCR.
Abstract: The exceptionally high prevalence of G1896A in FH and HCC demonstrates that the precore mutants are strongly associated with the progression of liver diseases in patients with HBeAg negative serology.
Abstract: The findings are also suggestive of sc
BCP/PC mutation prevalence and their association with HBV replication in HIV/HBV co-infected patients.
Abstract: A1762T, G1764A and G1896A mutations were common mutations identified in the BCP/PC region.
Abstract: However, the prevalence of the G1896A mutation was significantly high among the HBeAg negative HIV/HBV co-infected patients, and may be associated with high HBV replication.
LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B.
1Abstract: Association of the pcG1896A mutation with time to undetectable HBV-DNA, hepatitis B ""e"" antigen (HBeAg) seroclearance (in HBeAg-positive patients), and hepatitis B surface antigen (HBsAg) seroclearance was evaluated using Cox proportional hazards regression."
Abstract: Baseline pcG1896A mutation was identified in 51 (59.3%) patients, who were more commonly HBeAg-negative (P < .001) and had basal core promotor A1762T/G1764A mutations (P < .001).
Abstract: Cumulative proportion of undetectable HBV-DNA was significantly higher in patients
Fulminant hepatitis B virus (HBV) infection in an infant following mother-to-child transmission of an e-minus HBV mutant: Time to relook at HBV prophylaxis in South African infants.
Abstract: Genetic analysis of virus from mother and infant showed that both had the G1896A mutation in the preC/C gene, which truncates hepatitis e antigen (HBeAg) during translation, causing an HBeAg-negative phenotype.
Expansion of viral variants associated with immune escape and impaired virion secretion in patients with HBV reactivation after resolved infection.
Introduction: We previously demonstrated that resolved HBV carriers with the G1896A variant (guanine to adenine mutant at nucleotide 1896) in the precore gene of the HBV genome might have an increased risk of HBV reactivation and fatal acute liver failure.
Clinical features and viral quasispecies characteristics associated with infection by the hepatitis B virus G145R immune escape mutant.
Result: With regard to the 'hot-spot' mutations in the HBV genome, G1896A in the preC region and A1762T/G1764A in the basic core promoter region were studied.
Differential regulation of hepatitis B virus core protein expression and genome replication by a small upstream open reading frame and naturally occurring mutations in the precore region.
Abstract: G1896A nonsense mutation promoted more efficient core protein expression than mutated precore ATG, while a +1 frameshift mutation was ineffective.
Result: As for the alphalM0 +36 series, the replication impact of the G1896A mutation was mild.
Result: Comparison of alphalM0, F (alphalM0 with mutated precore ATG), and alphal in the same blot indicates that G1896A/G1899A were more effective than mutated precore ATG in augmenting core protein expression, although ol+36 did not show higher core protein level than F+36.
Result: Considering that genotype G harbors two nonsense mutations in the PMID: 28088502
2017
Infection, genetics and evolution
Abstract: The mutation rates of A1762T/G1764A and G1896A were found to decrease from 46.2% (24/52) at baseline to 36.5% (19/52) at week 12 (P=0.426) and from 28.8% (15/52) to 21.2% (11/52) (P=0.497), respectively.
A novel hepatitis B virus subgenotype D10 circulating in Ethiopia.
HBV mutation literature information.
PMID: 
2018
Saudi journal of biological sciences
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