Hepatitis B virus genotypes and precore mutations in Scottish blood donors

  1. F. Davidson1,*,
  2. C. Lycett1,
  3. E. Sablon2,
  4. J. Petrik1,
  5. B. C. Dow3

Article first published online: 17 FEB 2005

DOI: 10.1111/j.1423-0410.2005.00597.x

Issue

Vox Sanguinis

Vox Sanguinis

Volume 88, Issue 2, pages 87–92, February 2005

Additional Information

How to Cite

Davidson, F., Lycett, C., Sablon, E., Petrik, J. and Dow, B. C. (2005), Hepatitis B virus genotypes and precore mutations in Scottish blood donors. Vox Sanguinis, 88: 87–92. doi: 10.1111/j.1423-0410.2005.00597.x

Author Information

  1. 1

    Transfusion Transmitted Infection Group, Scottish National Blood Transfusion Service, Royal (Dick) Veterinary School, Edinburgh, UK

  2. 2

    Innogenetics N.V., Ghent, Belgium

  3. 3

    Microbiology Reference Unit, Scottish National Blood Transfusion Service, West of Scotland Transfusion Centre, Glasgow, UK

*Correspondence: Fiona Davidson, Transfusion Transmitted Infection Group, Scottish National Blood Transfusion Service, Royal (Dick) Veterinary School, Summerhall, Edinburgh EH9 1QH, UK E-mail: fiona.davidson@snbts.csa.scot.nhs.uk

Publication History

  1. Issue published online: 17 FEB 2005
  2. Article first published online: 17 FEB 2005
  3. Received: 21 July 2004, revised 14 October 2004, accepted 1 November 2004

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Keywords:

  • core promoter mutations;
  • HBV genotypes;
  • line probe assay;
  • precore mutations

Background and Objectives  This study was carried out to determine the frequency of hepatitis B virus (HBV) core promoter variants (nucleotide positions 1762, 1764) and precore variants (nucleotide position 1896) in hepatitis B surface antigen (HBsAg)-positive Scottish blood donors. HBV genotypes present in this population were also indentified.

Materials and Methods  A total of 85 HBsAg-positive blood donor samples were included in the study. Of these, 79 were polymerase chain reaction (PCR) positive and had sequence and mutation information. They were divided into two groups: group 1 (23 individuals) were hepatitis B e antigen (HBeAg)-positive and negative for antibody to HBe (anti-HBe); and group 2 (56 individuals) were HBeAg negative and positive for anti-HBe. A line probe assay was used to detect mutations, and a comparison was made by using direct sequence analysis. A different line probe assay was used to identify HBV genotype.

Results  The frequencies of mutations in group 1 were 22% each for mutations 1762, 1764 and 1896, increasing to 26%, 35% and 55% in group 2, respectively. By contrast, direct sequence analysis failed to identify 70% of wild-type/mutant mixes. The prevalence of viral genotypes was 41% for genotype A, 12% for genotype B, 5% for genotype C, 30% for genotype D and 12% for mixed-genotype infections. Precore mutations were seen in 10%, 88%, 25% and 74% of genotypes A, B, C and D, respectively.

Conclusions  The results indicate that core promoter and/or precore mutants may be under-reported. The combination of HBV PCR and line probe assays is useful for supplementing HBV serological tests. Non-Caucasian genotypes are present in the UK blood-donating population and will therefore affect the demographics of HBV infection.

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