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 HBV mutation literature information.


  Fulminant reactivation of hepatitis B due to envelope protein mutant that escaped detection by monoclonal HBsAg ELISA.
 PMID: 7539089       1995       Lancet (London, England)
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].
 PMID: 7553156       1995       Zhonghua yi xue za zhi
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.
 PMID: 7557146       1995       Gastroenterology
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.
 PMID: 7636505       1995       Journal of medical virology
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.
 PMID: 7645207       1995       Virology
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.
 PMID: 7730438       1995       Journal of virological methods
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.


  Hepatitis B virus strains with mutations in the core promoter in patients with fulminant hepatitis.
 PMID: 7825758       1995       Annals of internal medicine
Abstract: RESULTS: A point mutation from G to A at nucleotide 1896 in the precore region was detected in 519 (98%) of 529 HBV DNA clones from 38 patients.
Abstract: Two point mutations in the core promoter, from A to T at nucleotide 1762 and from G to A at nucleotide 1764, were detected in all 130 clones from the remaining 5 patients, who did not have mutations in the precore region, and in 20 (63%) of 32 clones from a patient with chronic hepatitis B who had transmitted HBV to 1 of these other 5 patients.



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