HBV mutation literature information.


  Glycine-to-arginine substitution at codon 145 of HBsAg in two infants born to hepatitis B e antigen-positive carrier.
 PMID: 7895545       1995       Digestive diseases and sciences
Abstract: Amino acid residues 122-160 of HBsAg were identical between the daughters and their mother except for a glycine-to-arginine substitution at codon 145.


  Probable implication of mutations of the X open reading frame in the onset of fulminant hepatitis B.
 PMID: 8551270       1995       Journal of medical virology
Abstract: A C-to-T substitution was found at nucleotide (nt) 1655, an A-to-T substitution at nt 1764 and a G-to-A substitution at nt 1766 in 4, 5 and 5 patients, respectively, out of the seven with fulminant hepatitis.


  A family cluster of an immune escape variant of hepatitis B virus infecting a mother and her two fully immunized children.
 PMID: 8574843       1995       Clinical and diagnostic laboratory immunology
Abstract: A hepatitis B virus (HBV) immune escape variant which results from a substitution of glycine by arginine at position 145 (arginine-145) in the immunodominant neutralization epitope of the S protein was found to infect one child in a seroepidemiologic survey of 1,812 vaccinated children.


  Emergence of hepatitis B virus S gene mutant in a liver transplant recipient.
 PMID: 8636711       1995       Journal of medical virology
Abstract: A double mutation generating an amino acid change (glycine to lysine) at residue 145, able to impair recognition by monoclonal antibodies, was observed in the post-transplant serum from one patient.


  Hepatitis B virus strains in Thailand: genomic variants in chronic carriers.
 PMID: 8636719       1995       Journal of medical virology
Abstract: Glycine 145 was changed to alanine in one strain, and this position showed an apparent mixture of glycine and arginine in another.


  Mutations in the core promoter/enhancer II regions of naturally occurring hepatitis B virus variants and analysis of the effects on transcription activities.
 PMID: 8724860       1995       Intervirology
Abstract: Predominant mutations were found to occur naturally in nucleotide positions 1762 (A to T) and 1764 (G to A) in chronic hepatitis patients and in asymptomatic carriers after seroconversion, but were not observed in HBeAg-positive healthy carriers.


  [Genetic variation in the cleavage site of the precore region of hepatitis B virus in Chinese patients with fulminant hepatitis].
 PMID: 8731842       1995       Zhonghua nei ke za zhi
Abstract: Double amino acid substitutions were seen in the precore region in the isolates: one from glycine to aspartic acid at codon 29 previously reported; the other substitution of phenylalanine for valine at codon 17 in the cleavage site of hepatitis B virus.


  A new immune escape mutant of hepatitis B virus with an Asp to Ala substitution in aa144 of the envelope major protein.
 PMID: 8834756       1995       Research in virology
Abstract: A new hepatitis B virus (HBV) mutant with an Asp to Ala substitution in aa144 of the envelope major protein was identified from the blood samples of two persistently infected patients.


  The precore/core promoter mutant (T1762A1764) of hepatitis B virus: clinical significance and an easy method for detection.
 PMID: 8847524       1995       The Journal of general virology
Abstract: Recently, a new hepatitis B virus (HBV) mutant with HBe antigen-negative phenotype has been characterized, in which one TATA box-like motif of the precore/core promoter had degenerated: most frequently by both A-->T and G-->A mutations at positions 1762 and 1764, respectively.


  Detection of hepatitis B precore mutants by the fluorescent linear polymerase chain reaction sequencing method.
 PMID: 7699256       1994       Journal of hepatology
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



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