Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital.
Abstract: One isolate (Irish-13), collected from a patient with acute asymptomatic infection, had a G1896A mutation and a 243 bp deletion of the polymerase gene.
Abstract: Only four isolates from patients with severe HBV infection harbored the G1896A stop codon mutation.
Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma.
PMID: 18695135
2008
Journal of the National Cancer Institute
Abstract: Among participants with a baseline HBV DNA level of at least 10(4) copies/mL, HCC incidence per 100 000 person-years was higher for those with the precore G1896 (wild-type) variant than for those with the G1896A variant (955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9]) and for those with the BCP A1762T/G1764A double mutant than for those with BCP A1762/G1764 (wild-type) variant (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% CI = 255.1 to 490.4]).
Abstract: Participants who had a baseline serum HBV DNA level greater than 10(4) copies/mL (n = 1526) were tested for the precore G1896A and PMID: 18803358
2008
World journal of gastroenterology
Abstract: The G1896A precore (PC) mutant was detected in 58.1% patients.
Virologic characteristics of hepatitis B virus in patients infected via maternal-fetal transmission.
PMID: 18837083
2008
World journal of gastroenterology
Abstract: The 1762T/1764A double mutation existed in all clones of the mother, 3 of them were also coupled with G1896A mutation, but none were found in the son.
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.
PMID: 18844615
2008
The American journal of gastroenterology
Introduction: The common precore mutation (G1896A), mutations in enhancer II (C1653T) and the basal core promoter (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.
Molecular epidemiology of hepatitis B virus in Iran.
PMID: 18844687
2008
Clinical microbiology and infection
Abstract: HBsAg (17.2%), precore-G1896A (59.5%) and Basal core promoter (BCP) double mutations (49.2%), whereas no recombination was found.
[A study on the relationship between point mutation in pre-core region G1896A of hepatitis B virus and safety of breast feeding].
PMID: 19178836
2008
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
Abstract: CONCLUSION: The point mutation in pre-core region G1896A of HBV dose not affect the positive rate of HBV DNA in breast milk and higher HBV DNA loads in serum of pregnant women might increase the risk of mother-infant transmission.
Abstract: OBJECTIVE: To investigate the relationship between pre-core G1896A point mutation of hepatitis B virus (HBV) and safety of breast feeding.
Abstract: PCR-solid phase hybridization was used to detect the point mutation in pre-core region G1896A of HBV from pregnant women, and HBV DNA loads in sera and breast milk were determined by fluorescence quantitative PCR (FQ-PCR).
Regulation of Toll-like receptor-2 expression in chronic hepatitis B by the precore protein.
Abstract: These results were confirmed in vitro using hepatic cell lines transduced with recombinant HBV baculovirus expressing wild-type HBV (HBeAg-positive), precore stop codon (G1896A) mutant HBV (HBeAg-negative).
Genotype and variations in core promoter and pre-core regions are related to progression of disease in HBV-infected patients from Northern Vietnam.
PMID: 17203204
2007
International journal of molecular medicine
Abstract: The rates of HBeAg seroconversion and G1896A for genotype B were significantly higher than those for genotype C (P<0.05).
Prevalence of hepatitis B virus genotype D in precore mutants among chronic liver disease patients from New Delhi, India.
PMID: 17211692
2007
Digestive diseases and sciences
Abstract: Our objective in this study was to genotype and detect the precore mutant with a point mutation from G to A at nucleotide 1896 using ligase chain reaction (LCR) and direct sequencing.