Abstract: Precore variants were detected in one HBeAg positive and in all 20 anti-HBe positive patients: in 19 cases, G to A at position 1896, with or without the substitution G to A at position 1899, in two cases C to T substitution at position 1817 which also produces a stop codon (CAA to TAA), one accompanied by the mutation G to A at position 1896.
Abstract: The only mutation observed in the patient who was initially HBeAg positive patient was a G to A substitution at position 1899.
Abstract: These results indicate that the main cause of non-expression of HBeAg in chronic hepati
Mutations in the transcriptional regulatory region of the precore and core/pregenome of a hepatitis B virus with defective HBeAg production.
Abstract: The deduced amino acid substitutions were 28 Arg--Gln, 94 His--Tyr, 131 Val--Ile and 132 Phe--Tyr of HBx and 715 Met--Val and 789 Asp--Asn of pol.
Different prevalence of precore mutants in five members of a hepatitis-B-virus-infected family: evidence for a precore variant type in an asymptomatic anti-HBs patient.
Abstract: A method for rapid screening of a large number of cloned polymerase chain reaction products was developed for the presence of the most frequent pre-C mutations (G to A substitution at nucleotide position 1896 and 1899).
The role of pre-core hepatitis B virus mutants on the long-term outcome of chronic hepatitis B virus hepatitis. A longitudinal study.
Abstract: Anti-HBe seroconversion was accompanied by a dramatic reduction of hepatitis B virus replication and normalization of alanine aminotransferase in all, except one, and by the emergence of mutated strains with a pre-core stop codon (point mutation G to A at nt 1896) that replaced the wild type in seven of the 12.
Hepatitis B virus with mutations in the core promoter for an e antigen-negative phenotype in carriers with antibody to e antigen.
Abstract: Two point mutations in the core promoter, from A to T at nt 1762 and from G to A at nt 1764, were most prevalent.
Nucleotide sequence analysis of the precore region in patients with spontaneous reactivation of chronic hepatitis B.
PMID: 8082510
1994
Digestive diseases and sciences
Abstract: Prior to reactivation, none of the group I patients harbored an HBV strain having a mutation that prevented HBeAg synthesis; however, 2/5 developed such a mutation during reactivation (G to A transition at nt 1896).
Mutation specific PCR and direct solid phase sequencing assay for the detection of hepatitis B virus pre-C/C mutants in anti-HBe-positive, chronic hepatitis B.
Abstract: Sequence analysis of the HBV DNA from patients with anti-HBe+, chronic hepatitis B revealed that the lack of HBeAg is mostly due to a single G-->A transition at nucleotide position 1896, resulting in a translational stop codon.
A novel hepatitis B virus variant in the sera of immunized children.
PMID: 8113769
1994
The Journal of general virology
Abstract: A unique nucleotide change from adenosine to guanosine at nucleotide 421 was found, resulting in an amino acid substitution at residue 141 from lysine to glutamic acid.
Mutations in the pre-core region of hepatitis B virus serve to enhance the stability of the secondary structure of the pre-genome encapsidation signal.
Abstract: Four major missense/nonsense mutations (M) were found: (M1) C-->T at nucleotide position 1856, Pro-->Ser at codon 15; (M2) G-->A at position 1896, Trp-->stop at codon 28; (M3) G-->A at position 1898, Gly-->Ser at codon 29; and (M4) G-->A at position 1899, Gly-->Asp at codon 29.
Abstract: The commonest conserved mutation was M0: T-->C at position 1858, Pro-->Pro at codon 15.
Detection of precore hepatitis B virus mutants in asymptomatic HBsAg-positive family members.
Abstract: M0, a conserved mutation (T-to-C at nucleotide 1858, codon 15), was detected in 81% and 12% family members of index patients with and without M0, respectively (p < 0.0001).
Abstract: We previously reported two novel mutations: M1 (C-to-T change at nucleotide 1856 [proser at codon 15]) and M3 (G-to-A change at nucleotide 1898 [gly-ser at codon 29]) in addition to two well-described mutations: M2 (G-to-A change at nucleotide 1896 [trp-stop at codon 28]); and M4 (G-to-A change at nucleotide 1899 [gly-asp at codon 29]) in Chinese patients.
HBV mutation literature information.
PMID: 
1994
Journal of hepatology
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