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).
Identification of HBV DNA sequences that are predictive of response to lamivudine therapy.
Abstract: Reversions of precore mutations A1762T/G1764A and G1896A were observed in 29% and 25% of patients, respectively, but none became HBeAg-positive.
Fibrosing cholestatic hepatitis secondary to precore/core promoter hepatitis B variant with lamivudine resistance: successful retransplantation with combination adefovir dipivoxil and hepatitis B immunoglobulin.
Abstract: Analysis of gene sequence variation by polymerase chain reaction (PCR) and direct sequencing showed that both had a core promoter variant A1762T/G1764A and 1 had a concomitant precore stop codon G1896A variant in prelamivudine and postrecurrence serum samples.
[Emergence and clinical significance of YMDD and HBeAg-related mutations during lamivudine treatment].
Abstract: 3 of the 8 patients had G1896A mutant, 2 had A1814C and the remaining had G1896A + A1814C, A1762T and G1764A, A1762T and G1764A + G1896A.
Abstract: METHODS: From sera of chronic hepatitis B patients with 9 - 30 months lamivudine therapy, signal-base mutations of YMDD motif, G1896A, A1814C, A1762T and G1764A were analyzed by gene chips technique.
Real-time quantification of hepatitis B virus core-promoter and pre-core mutants during hepatitis E antigen seroconversion.
Abstract: BACKGROUND/AIMS: Detection of hepatitis B virus (HBV) core-promoter A(1762)T-G(1764)A and pre-core G(1896)A mutants has relied on qualitative assays.
Abstract: CONCLUSIONS: The A(1762)T-G(1764)A and G(1896)A mutants existed in a high proportion of patients before and were unaffected after HbeAg seroconversion.
Abstract: Quantity of A(1762)T-G(1764)A mutants was positively correlated with alanine aminotransferase (ALT) (P<0.001) and HBV DNA (P<0.001) levels, both before and after HBeAg seroconversion.
Abstract: RESULTS: Sig
Polyarteritis nodosa associated with hepatitis B virus infection. The role of antiviral treatment and mutations in the hepatitis B virus genome.
PMID: 15256984
2004
European journal of gastroenterology & hepatology
Abstract: In one patient a stop codon in the pre-core region and a double mutation A1762T-G1764A were found during antiviral therapy.
Basal core promoter and precore mutations in the hepatitis B virus genome enhance replication efficacy of Lamivudine-resistant mutants.
Abstract: The PC mutation (G1896A+C1858T) creates a translational stop codon resulting in absent HBeAg expression, whereas BCP mutations (A1762T/G1764A) reduce HBeAg expression by transcriptional mechanisms.
[Full-length sequence of hepatitis B virus isolated from high incidence hepatocellular carcinoma area-Longan county].
PMID: 15640866
2004
Zhonghua shi yan he lin chuang bing du xue za zhi
Abstract: Six point mutations including the double mutations (nt 1762 A to T, 1764 G to A) were found in X gene leading to 4 amino acids change.
Lamivudine and Famciclovir resistant hepatitis B virus associated with fatal hepatic failure.
Abstract: Subsequent to the instigation of antiviral therapy, the dominant drug resistant HBV which caused virological breakthrough and was associated with hepatic failure displayed a series of unique mutations particularly in the BCP (A1762T and G1764A) and in the polymerase (rtL180M, rtM204V, rtA222T and rtL336V), core (cP5T, cS26A,
HBV mutation literature information.
PMID: 
2005
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