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.
Fulminant reactivation of hepatitis B due to envelope protein mutant that escaped detection by monoclonal HBsAg ELISA.
Abstract: PCR sequencing revealed a substitution of arginine for glycine at position 145 of HBsAg in the major neutralising epitope cluster, the a determinant, as well as a 2-aminoacid insertion of asparagine and threonine between positions 122 and 123, immediately upstream of this determinant.
[Expression of 12 antibody escape mutants of hepatitis B virus surface antigen gene in mammalian cell by using an Epstein-Barr based vector].
Abstract: The results of detection of HBsAg excreted by resistant cell clones with monoclonal antibody to HBsAg showed that all antibody escape mutants of HBsAg except mutant 145R, a substitution of arginine for glycine at amino acid 145 position in HBsAg, were positive.
Hepatitis B virus core promoter sequence analysis in fulminant and chronic hepatitis B.
Abstract: BACKGROUND & AIMS: It was recently reported that two point mutations within the hepatitis B virus (HBV) core promoter region (A to T at position 1762 and G to A at position 1764) are associated with fulminant hepatitis and lead to hepatitis B e antigen (HBeAg)-negative phenotype.
Mutations of some critical amino acid residues in the hepatitis B virus surface antigen.
Abstract: Mutation of cysteine 149 to serine or of glycine 145 to arginine (imitating naturally occurring mutants), lysine, or glutamatic acid all led to loss of cross-reactivity with polyclonal antisera.
The mechanism of natural occurrence of two closely linked HBV precore predominant mutations.
Abstract: At nt 1899, a G to A mutation changes glycine at codon 29 to aspartic acid.
Abstract: The preferential occurrence of the G to A mutation at nt 1896 and 1899, instead of at other nonpredominant positions, is likely to be a combined consequence of both selection and higher intrinsic mutation frequency at these positions.
Precore mutant of hepatitis B virus in childhood fulminant hepatitis B: an infrequent association.
PMID: 7706802
1995
The Journal of infectious diseases
Abstract: A precore mutation from G to A at nucleotide 1896 was found in 5 of 14 FHB patients and in 3 of 10 AHB patients.
Demonstration of the presence of protease-cutting site in the spacer of hepatitis B viral Pol protein.
Abstract: By using a novel method called the LacZ localization assay (LLA), it was demonstrated that a tripartite fusion protein containing the nucleus localization sequence (NLS) of SV40 large T Ag, the putative thrombin cutting sequence (Ile-Arg-Ile-Pro-Arg320-Thr) of HBV Pol protein and the full length beta-galactosidase of E.
Detection of hepatitis B virus precore TAG mutant by an amplification-created restriction site method.
PMID: 7798663
1995
The Journal of infectious diseases
Abstract: A new method for detecting the hepatitis B virus (HBV) precore 1896 G-->A mutation is described.
Abstract: This method of detecting HBV precore 1896 G-->A should be useful for evaluation and follow-up of patients and for prevalence studies.
Nucleotide sequence analysis of precore and proximal core regions in patients with chronic hepatitis B treated with interferon.
PMID: 7821093
1995
Digestive diseases and sciences
Abstract: Mutations that prevent HBeAg synthesis were found in three patients, all of whom had G-to-A substitution at nt 1896 and two of them were anti-HBe positive.
HBV mutation literature information.
PMID: 
1995
Hepatology (Baltimore, Md.)
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