literature

HBV mutation literature information.

A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C. Japan HBV Genotype Research Group.

PMID: 11124839 2001 Hepatology (Baltimore, Md.)

Abstract: The predominance of mutants with G-to-A mutation at nucleotide (nt) 1896 in the precore region (A1896) over the wild-type was comparable between genotype B and C patients (60% and 62%, respectively), and it correlated with anti-HBe.

Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers.

PMID: 11472634 2001 BMC microbiology

Abstract: BACKGROUND: Mutations in the core promoter and precore regions of the hepatitis B virus (HBV) genome, notably the double substitution (AGG to TGA) at nt positions 1762-1764 in the core promoter, and the precore stop codon mutation G to A at nt 1896, can often explain the anti-HBe phenotype in chronic carriers.

Result: The seven others (five from genotype D and two from genotype F) showed the 1896 G to A substitution leading to a stable T1858:A1896 base pairing and introducing a stop codon into the ORF of th

Discussion: The most common mutation was the G to A change at nt 1896 that creates a stop codon in the precore ORF.

Phylogenetic origin of hepatitis B virus strains with precore C-1858 variant.

PMID: 11526151 2001 Journal of clinical microbiology

Abstract: The predominant mutation, the precore G-->A-1896 mutation, is restricted by the variability at position 1858 and is rare in strains with cytosine at nucleotide 1858.

Reactivation of latently infected hepatitis B virus in a leukemia patient with antibodies to hepatitis B core antigen.

PMID: 11578069 2001 Journal of gastroenterology

Abstract: Mutation-specific assay based on competitive polymerase chain reaction (PCR) and sequencing analyses revealed the predominant reactivation of an HBV strain with missence mutation (point mutation G-to-A at nucleotide 1896) in the precore regions, as well as point mutations in the core promoter regions.

Hepatitis B virus harboring nucleotide deletions in the core promoter region and genotype B correlate with low viral replication activity in anti-HBe positive carriers.

PMID: 11595588 2001 Journal of clinical virology

Abstract: RESULTS: Various mutations were detected including C to T point mutation at nt 1653, A to T and G to A contiguous point mutations at nt 1762 and 1764 in the core promoter region, and G to A point mutation at nt 1896 in the precore region, but no common mutations were detected that were directly related to the virus titer from earlier reported mutations.

Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B.

PMID: 11596083 2001 Journal of medical virology

Abstract: G1896A was, however, present in the one genotype D isolate.

Abstract: A relatively large number of mutations were present in the middle region of the core gene in those isolates without G1896A or A1762T, G1764A mutations, although the pattern was not consistent with those in published studies.

Abstract: The mutation most often reported in patients with fulminant hepatitis B, the G1896A precore stop-codon substitution, was, as expected, not present in the genotype A isolates with the exception of one in which it was accompanied by a compensatory C1858T substitution.

Hepatitis B virus genomes of chronic hepatitis patients do not contain specific mutations related to acute exacerbation.

PMID: 11680583 2001 Digestive diseases and sciences

Abstract: A 1896 precore stop codon mutant (G to A at nt 1896) coexisting with the wild sequence was found in both patients prior to seroconversion from HBeAg to anti-HBe.

Reactivation of precore mutant hepatitis B virus in chemotherapy-treated patients.

PMID: 11753968 2001 Cancer

Abstract: A point mutation from G to A at nt 1896 was detected in five of these six patients.

Abstract: BACKGROUND: A point mutation from G to A at nucleotide (nt) 1896 of the precore region of hepatitis B virus (HBV) DNA has been shown to be associated with fulminant and severe hepatitis.

Abstract: Prophylactic use of lamivudine is strongly recommended for patients who carry mutant HBV at precore region, especially at nt 1896 (G to A), before and during chemotherapy.

Base-pair alterations in the epsilon-lower stem due to a novel double substitution in the precore gene of HBV-e negative variant were recovered by secondary mutations.

PMID: 11778699 2001 Virus genes

Abstract: The HBe negative phenotype, a natural precore mutant (G1896A/G1897A) of HBV with aborted HBeAg expression is known to cause chronic hepatitis.

Abstract: The destabilized C : G base-pairing in the lower stem of epsilon-hairpin due to G1896A substitution is reportedly compensated by a second C1858T mutation and suggested to play an important role in enhanced selection of the HBe negative variant.

Abstract: Three of the 5 HBe negative patients had classical G1896A mutation having a second compensatory mutation at nt.

Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: precore/core mutations may play an important role.

PMID: 10630955 2000 Journal of medical virology

Abstract: In each case, similar mutations (G to A) in nucleotide 1896 of the preC region were found, together with additional mutations in the preC promoter.

Abstract: Patients who are chronic carriers of the HBV and who have a G to A mutation at nucleotide 1896 in the precore region may develop more severe liver disease, possibly because of rapid selection and enhanced replication ability of the mutant strain.

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