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 HBV mutation literature information.


  Hepatitis B virus carriers without precore mutations in hepatitis B e antigen-negative stage show more severe liver damage.
 PMID: 8781313       1996       Hepatology (Baltimore, Md.)
Abstract: The G-->A mutation at nucleotide 1896 may mediate viral escape by creating a TAG stop codon in the precore region, thus preventing HBeAg production.


  Rare pre-core stop-codon mutant nt. 1897 predominates over wide-spread mutant nt. 1896 in an unusual course of chronic hepatitis B.
 PMID: 8871875       1996       Journal of viral hepatitis
Abstract: Direct sequencing of polymerase chain reaction (PCR) products derived from consecutive sera showed a rare pre-core stop-codon mutation at nucleotide (nt.) 1897 G --> A with an accompanying mutation nt. 1857 C --> T as well as a stop-codon mutation nt. 1896 G --> A.


  The mechanism of natural occurrence of two closely linked HBV precore predominant mutations.
 PMID: 7645207       1995       Virology
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.


  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.


  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: These results indicate that the main cause of non-expression of HBeAg in chronic hepatitis B in our country is the substitution of G to A at nucleotide 1896, alone or accompanied by other variants.


  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.
 PMID: 7890897       1994       Journal of hepatology
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.
 PMID: 7930478       1994       Journal of hepatology
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.



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