Two core promotor mutations identified in a hepatitis B virus strain associated with fulminant hepatitis result in enhanced viral replication.
PMID: 8941643
1996
The Journal of clinical investigation
Abstract: Analysis of viral replication showed that two adjacent mutations in the HBV core promotor (C to T at nucleotide 1768 and T to A at nucleotide 1770) led to high level replication.
[Detection of hepatitis B virus by using polymerase chain reaction and nonradioactive DNA probes. II. Identification of mutations in the core gene by PCR-direct sequencing and ASO probe method].
Abstract: The analysis of nucleotide sequences (codon 27-100) of HBV DNA in anti-HBe positive sera showed that there were two hypervariable segments of codon 31-49 and codon 87-97, where amino acid substitutions of L31I, S49T, S87G/N, K96N and I87F/1 frequently occurred regardless of the presence or absence of the mutation in the pre-core region.
Reduced precore transcription and enhanced core-pregenome transcription of hepatitis B virus DNA after replacement of the precore-core promoter with sequences associated with e antigen-seronegative persistent infections.
Abstract: The mutant with coexisting A1762T and G1764A substitutions produced less than one-fifth of the wild-type level of HBeAg.
Semiquantitative assessment of pre-core stop-codon mutant and wildtype hepatitis B virus during the course of chronic hepatitis B using a new PCR-based assay.
Abstract: Especially, A to T mutations at nucleotide 1762 and G to A mutations at nucleotide 1764 were found in five anti-HBe-positive asymptomatic carriers, and 22 patients with chronic liver disease.
Pathogenesis of chronic liver disease in patients with chronic hepatitis B virus infection without serum HBeAg.
PMID: 9011456
1996
Digestive diseases and sciences
Abstract: Chronic hepatitis B in patients lacking hepatitis B e antigen has been attributed to a hepatitis B virus variant (G-to-A mutation at nucleotide 1896 in the precore region of the genome).
Increasing heterogeneity of the 'a' determinant of HBsAg found in the presumed late phase of chronic hepatitis B virus infection.
PMID: 9122641
1996
Scandinavian journal of infectious diseases
Abstract: Most prevalent was a point mutation from adenine to guanine at nucleotide 530 resulting in a change from threonine to alanine at amino acid position 126.
[Genomic heterogeneity of hepatitis B virus, genotype A circulating in the metropolitan area of Buenos Aires, Argentina].
Abstract: pHB4 shows a mutation at the T 3182-Leu in the preS1 region that change Pro for Leu, this mutation is absent in 125 sequences selected (having a 65% or more of homology) from NCBI by Blast algortm.
[Detection of hepatitis B virus by using polymerase chain reaction and nonradioactive DNA probes. I. Identification of mutations in the precore region by PCR-direct sequencing and ASO probe method].
PMID: 7474444
1995
Rinsho byori. The Japanese journal of clinical pathology
Abstract: Five unknown mutations (I10N, C12W, C14S, V17F and A19D), three known mutations (I9V, W28X and G29D) and for novel nucleotide insertions were identified in anti-HBe positive sera.
Abstract: The W28X mutation was found in anti-HBe positive but not in any of HBeAg positive sera.
Hepatitis B virus infection: precore mutants and its relation to viral genotypes and core mutations.
Abstract: In genotype A, the M1 mutation coexisted with a second mutation (C-->T at position 1858 in codon 15), and both mutations were paired in the secondary structure of the RNA encapsidation signal, which justified the rare presence of precore mutants in this genotype.
HBV mutation literature information.
PMID: 
1996
The Journal of clinical investigation
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