HBV mutation literature information.


  Variant of hepatitis B virus isolated in Zimbabwe.
 PMID: 8308523       1994       Journal of medical virology
1Abstract: Within the second loop of the ""a"" determinant, two mutations resulting in substitution of serine or threonine with the hydrophobic amino acids, methionine at position 143 and with alanine in place of glycine at position 145, are predicted from the consensus nucleotide sequence of the PCR-derived clones."


  Fibrosing cholestatic hepatitis in a transplant recipient with hepatitis B virus precore mutant.
 PMID: 8359657       1993       Gastroenterology
Abstract: Sequencing of the HBV precore region of the pretransplant serum sample confirmed the presence of the precore stop-codon mutant (G-->A mutation in codon 1896) only.


  Nucleotide sequence analysis of the precore region in patients with fulminant hepatitis B in the United States.
 PMID: 8405863       1993       Gastroenterology
Abstract: RESULTS: Four patients (10.8%) harbored nonsense mutants likely to produce an HBeAg negative HBV infection; two such mutants had a G to A substitution at position 1896, one lost the precore initiation codon, and one harbored a stop codon immediately downstream of the precore initiation codon.


  "Loss of the common ""A"" determinant of hepatitis B surface antigen by a vaccine-induced escape mutant."
 PMID: 1281839       1992       The Journal of clinical investigation
Abstract: A substitution of arginine for glycine at amino acid 145 in HBsAg was observed.


  Naturally occurring point mutation in the C terminus of the polymerase gene prevents duck hepatitis B virus RNA packaging.
 PMID: 1309904       1992       Journal of virology
Abstract: Using genetic approaches, it was determined that a change of cysteine to tyrosine in position 711 in the polymerase (P) gene C terminus led to this RNA-packaging defect.


  Association of hepatitis B viral precore mutations with fulminant hepatitis B in Japan.
 PMID: 1926786       1991       Virology
Abstract: We demonstrated that patients with fulminant hepatitis B carried HBV genomes with a G to A mutation at nucleotide positions 1898 (five of five patients; 18 of 18 clones, 100%) and 1901 (five of five patients; 12 of 18 clones, 66%) in the precore region.


  Mutations in the precore region of hepatitis B virus DNA in patients with fulminant and severe hepatitis.
 PMID: 2034246       1991       The New England journal of medicine
Abstract: RESULTS: Of the nine patients with fatal hepatitis, seven had retrievable hepatitis B DNA: In all seven there was a point mutation from G to A at nucleotide 1896 of the precore region, converting tryptophan (TGG) to a stop codon (TAG).


  Hepatitis B viruses with precore region defects prevail in persistently infected hosts along with seroconversion to the antibody against e antigen.
 PMID: 2304145       1990       Journal of virology
Abstract: A point mutation from G to A at nucleotide 83, converting Trp-28 (TGG) to a stop codon (TAG), was by far the commonest and was observed in HBV DNA clones from 16 (89%) of 18 carriers seropositive for anti-HBe.


  Mutations that change the immunological subtype of hepatitis B virus surface antigen and distinguish between antigenic and immunogenic determination.
 PMID: 2693611       1989       Journal of medical virology
Abstract: When combined with substitution of serine 113 by threonine, replacement of arginine 122 by lysine or of tyrosine 134 by phenylalanine, or both of these changes, altered the antigenic subtype of HBsAg from y+d- to y+d.


  Site-directed mutagenesis of hepatitis B surface antigen sequence at codon 160 from arginine to lysine for conversion of subtypic determinant from r to w.
 PMID: 3118876       1987       Biochemical and biophysical research communications
Abstract: These results indicate that a point mutation from G to A at nucleotide 479 in the S gene, changing codon 160 for arginine to that for lysine, can convert the subtypic determinant of hepatitis B surface antigen from r to its allelic determinant w.



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