Abstract: The A to T mutation at nucleotide 1762 and/or G to A mutation at nucleotide 1764 were found in 30% in HBeAg(+) ASC, 65.7% in inactive HBsAg carrier, 95% in chronic hepatitis B, and 90% in liver cirrhosis (p < 0.001).
Influence of genotypes and precore mutations on fulminant or chronic outcome of acute hepatitis B virus infection.
Abstract: Precore (G1896A) and core-promoter (A1762T/G1764A) mutations were more frequent in patients with fulminant than acute self-limited hepatitis (53% vs.
Abstract: In in vitro transfection experiments, the replication of Bj clone was markedly enhanced by introducing either G1896A or A1762T/G1764A mutation.
Association of core promoter mutations with viral breakthrough in chronic hepatitis B patients on long-term lamivudine therapy.
PMID: 16928212
2006
Journal of gastroenterology and hepatology
Abstract: Core promoter mutations were seen in five of eight (62.5%) and in six of nine (66.6%); classic double mutations (A1762T/G1764A) of core promoter region were detected in two and three patients and novel double mutations of core promoter (G1764T/C1766G) in one patient each of group Ia and Ib patients, respectively.
Three-phase sequential combined treatment with lamivudine and interferon in young patients with chronic hepatitis B.
Abstract: HBV mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found in the majority of cases, mutations that have previously been reported in HBV that is integrated in HCC DNA.
Abstract: In 18 of 21 (86%) patients with detectable HBV core promoter sequences, mutations at both nucleotides 1762 (A-GT) and 1764 (G-A) in the core promoter region were found.
High level of hepatitis B virus DNA after HBeAg-to-anti-HBe seroconversion is related to coexistence of mutations in its precore and basal core promoter.
PMID: 15918203
2005
World journal of gastroenterology
Abstract: AIM: G1896A mutation in precore or A1762T/G1764A mutations in basal core promoter are suspected to be responsible for patients with detectable level of HBV DNA in serum after seroconversion from HBeAg to anti-HBe.
Abstract: CONCLUSION: The coexistence of G1896A mutation and A1762T/G1764A mutations is very common, and responsible for the major cases w
Abstract: Coexistence mutations were found in 77.1% (64/83) out of sera with A1762T/G1764A mutations, and in 50.0% (64/128) out of sera with G1896A mutation.
Optimization of competitively differentiated polymerase chain reaction in detection of HBV basal core promoter mutation.
PMID: 15962387
2005
World journal of gastroenterology
Abstract: A1762T/G1764A mutant was detected in 41.8% (51/122) of patients with HBV infection, but not detected in controls with negative HBsAg.
Abstract: METHODS: Recombinant plasmid of double point mutation A1762T/G1764A in basal core promoter of HBV constructed by site-directed mutagenesis was used as mutant control.
Abstract: Optimized CD-PCR was evaluated by detecting A1762T/G1764A mutation in recombinant plasmids and clinical sera from patients with HBV infection.
Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis.
Abstract: Core promoter': the double basic core promoter (A1762T/G1764A) variant was detected in seven of eight (87%) of group A and in one of five (20%; P=0.03) of group B1 and one of nine (11%; P=0.002) of group B2 patients.
Hepatitis B virus DNA quantitation and detection of core promoter, precore and polymerase mutations in chronic hepatitis B: evaluation and clinical usefulness of three new commercial assays.
Abstract: affigene HBV mutant VL (positions G1764A, G1896A) and affigene HBV DE/3TC (positions rtL180M, rtM204V/I) were able to detect a low presence of mutants in a mixed population (wild type and mutant) compared to direct sequencing and Inno-LIPA HBV DR, which identified only the dominant population.
Early response to interferon alpha treatment and long-term clinical outcome in Japanese patients with chronic HBV genotype C infection.
PMID: 14654974
2004
International journal of molecular medicine
Abstract: 92%) and a higher frequency of core promoter mutation (A1762T/G1764A).
HBV mutation literature information.
PMID: 
2006
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