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.
LCR based quick detection of hotspot G1896A mutation in patients with different spectrum of hepatitis B.
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.
Novel assay of competitively differentiated polymerase chain reaction for screening point mutation of hepatitis B virus.
PMID: 12918112
2003
World journal of gastroenterology
Abstract: CD-PCR could detect one copy of G1896A variant among 10-100 copies of wild-type plasmid DNA.
Abstract: CD-PCR was evaluated by detecting G1896A variant of hepatitis B virus (HBV) in form of recombinant plasmids and in sera from patients with hepatitis B, and compared with allele-specific PCR (AS-PCR) and competitive AS-PCR.
Abstract: HBV G1896A or other more important mutations have to be routinely detected in patients with a detectable level of viremia after HBeAg/antibody conversion in clinical practice.
Abstract: HBV G1896A variant was more often found in HBeAg (-) patients with a lower level of detectable viremia than that with a higher level of detectable viremia (P=0.0192).
Abstract: It could clearly distinguish wild-type and mutant-type p
Prevalence of HBV precore/core promoter variants in the United States.
Abstract: Variants in the precore (G(1896)A) and core promoter (A(1762)T, G(1764)A) regions of hepatitis B virus (HBV) may be related to serum HBV DNA levels and severity of liver disease.
HBV mutation literature information.
PMID: 
2004
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