HBV mutation literature information.


  A case-control study for clinical and molecular biological differences between hepatitis B viruses of genotypes B and C. Japan HBV Genotype Research Group.
 PMID: 11124839       2001       Hepatology (Baltimore, Md.)
Abstract: The double mutation in the basic core promoter (A-to-T at nt 1762 and G-to-A at nt 1764), however, was significantly more frequent in genotype C than B patients (58% vs.


  Full-length genomic analysis of hepatitis B virus isolates in a patient progressing from hepatitis to hepatocellular carcinoma.
 PMID: 11424118       2001       Journal of medical virology
Abstract: High frequency of mutations at nucleotides 1762(A-->T) and 1764(G-->A) in the core promoter region have been described in HCC.


  Full-length genomic analysis of hepatitis B virus isolates in a patient progressing from hepatitis to hepatocellular carcinoma.
 PMID: 11468748       2001       Journal of medical virology
Abstract: High frequency of mutations at nucleotides 1762(A-->T) and 1764(G-->A) in the core promoter region have been described in HCC.


  Molecular analysis of hepatitis B virus genomes isolated from black African patients with fulminant hepatitis B.
 PMID: 11596083       2001       Journal of medical virology
Abstract: A relatively large number of mutations were present in the middle region of the core gene in those isolates without G1896A or A1762T, G1764A mutations, although the pattern was not consistent with those in published studies.
Abstract: The other mutation commonly found in patients with fulminant hepatitis B, the paired A1762T, G1764A substitution in the basic core promoter, was present in only one patient and G1764A in one other.


  Hepatitis B virus genomes of chronic hepatitis patients do not contain specific mutations related to acute exacerbation.
 PMID: 11680583       2001       Digestive diseases and sciences
Abstract: Core promoter mutations at nucleotide positions 1762 (A to T) and 1764 (G to A) were found in both patients throughout the observation period.


  Properties of hepatitis B virus genome recovered from Vietnamese patients with fulminant hepatitis in comparison with those of acute hepatitis.
 PMID: 10745228       2000       Journal of medical virology
Abstract: Of note as negative data, the mutations C1653T and T1753M of the enhancer II (Enh II) and A1762T and G1764A of the precore/core promoter regions, once reported to be relevant to severe or fulminant hepatitis, were not found in the present cases.


  Sequence variations of precore/core and precore promoter regions of hepatitis B virus in patients with or without viral reactivation during cytotoxic chemotherapy.
 PMID: 11115057       2000       Journal of viral hepatitis
Abstract: With respect to the preC promoter region, the two commonest mutations detected were at nt 1762 (A to T) and nt 1764 (G to A).


  Diversity of core promoter mutations in immune clearance phase of chronic HBV infection.
 PMID: 10514111       1999       European journal of gastroenterology & hepatology
Abstract: While mutations at nucleotide 1762 (A-->T) and 1764(G-->A) were not found in ASC, mutations at the same positions were found in all the cases of CH group (40 clones) (P=0.003).


  T1762/A1764 variants of the basal core promoter of hepatitis B virus; serological and clinical correlations in Chinese patients.
 PMID: 10533799       1999       Liver
Abstract: BACKGROUND: A double variant in the basal core promoter, converting nucleotide 1762 from A to T (T1762) and nucleotide 1764 from G to A (A[764), has been described in patients with chronic hepatitis B infection.


  Age at time of hepatitis Be antibody seroconversion in childhood chronic hepatitis B infection and mutant viral strain detection rates.
 PMID: 10554127       1999       Journal of pediatric gastroenterology and nutrition
Abstract: Specifically, a mutant strain showing a G-to-A substitution at nucleotide 83 in the pre-C region, or a mutant strain showing an A-to-T substitution at nucleotide 1762 and a G-to-A substitution at nucleotide 1764, was detected in only two of eight cases (25%) from the HBeAb-positive carriers with documented seroconversion before age 6.



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