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.
Sequential combination therapy of HBe antigen-negative/virus-DNA-positive chronic hepatitis B with famciclovir or lamivudine and interferon-alpha-2a.
Abstract: CONCLUSION: Sequential combination therapy can induce sustained virologic response in a subgroup of CHBe-, but most with the G1896A precore mutant HBV relapse.
Abstract: Most patients (5/7) with the G1896A mutation relapsed within 4 months after therapy.
Abstract: Only two of them had been infected by HBV with the G1896A mutation.
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 G(1896)A mutant was negatively correlated with ALT (P=0.044) and HBV DNA (P=0.007) levels.
Abstract: Significant quantities of pre-core G(1896)A mutant existed in about 90% of patients bef
Usefulness of dried blood samples for quantification and molecular characterization of HBV-DNA.
Abstract: The purpose of this study was to assess the use of dried blood spot (DBS) samples for hepatitis B virus (HBV) DNA quantification, HBV genotyping, and detection of G1896A precore mutants and variants in the YMDD polymerase motif.
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.
Effect of the G1896A precore mutation on drug sensitivity and replication yield of lamivudine-resistant HBV in vitro.
Abstract: HBV baculoviruses encoding the G1896A PC stop codon mutation were generated in wild-type (WT) and lamivudine-resistant (rtM204I and rtL180M + rtM204V) backgrounds, resulting in a panel of 6 related recombinant baculoviruses.
Abstract: Hepatitis B e antigen (HBeAg) negative chronic hepatitis B (CHB) is frequently caused by a mutation (G1896A) in the hepatitis B virus (HBV) precore (PC) reading frame that
Molecular epidemiology and transmission of hepatitis B virus in close family contacts of HBV-related chronic liver disease patients.
Abstract: G1896A mutation was found in 7 of 11 (64%) specimens changing amino acid tryptophane (W) to stop codon.
Abstract: The results of the study, demonstrate (1) clustering of Pre-C and S-gene mutations in the families, (2) horizontal mode of transmission and a common source infection appears to be frequent as evidenced by sequence homology and detailed history, (3) T118V and A128V were the commonest mutations in the S-gene region, while (4) M2 (G1896A) was the commonest pre-C gene mutation, and (5) long-term follow-up evaluation of these mutations suggested.
Analysis of clinical, biochemical and viral factors associated with early relapse after lamivudine treatment for hepatitis B e antigen-negative chronic hepatitis B patients in Taiwan.
Abstract: Precore (G1896A) and basic core promoter (BCP, A1762T & G1764A) mutations were determined by PCR and direct sequencing.
Abstract: G1896A was predominant in genotype B infected patients (95.2%vs 63.6%, P = 0.037).
The T(1858) variant predisposing to the precore stop mutation correlates with one of two major genotype F hepatitis B virus clades.
PMID: 12867638
2003
The Journal of general virology
Abstract: The precore mutation G(1896)-->A occurs frequently in anti-HBe-positive carriers of HBsAg with T(1858) in the stem of the encapsidation signal.
HBV mutation literature information.
PMID: 
2004
Liver transplantation
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