Polymorphisms of interleukin-1beta in Japanese patients with hepatitis B virus infection

J Hepatol. 2007 Mar;46(3):381-6. doi: 10.1016/j.jhep.2006.09.015. Epub 2006 Nov 2.

Abstract

Background/aims: Hepatitis B virus (HBV) induces liver cirrhosis (LC) and hepatocellular carcinoma (HCC) mainly by causing chronic necro-inflammatory hepatic disease. Our aim was to investigate the relationships between the polymorphisms of the interleukin-1B (IL-1B) promoter region and the interleukin-1 receptor antagonist gene (IL-1RN) and disease progression in an HBV-infected Japanese population.

Methods: Genomic DNA was extracted from the peripheral blood of 237 HBV carriers. Polymorphisms in IL-1B and IL-1RN were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR with confronting two-pair primers (PCR-CTPP) methods. These polymorphic sites include the promoter regions of IL-1B at positions -511 and -31, and IL-1RN variable tandem repeats.

Results: The IL-1B -31 and -511 loci were in complete linkage disequilibrium, and the frequency of the IL-1B -31 T carrier (IL-1B -31 T/T or T/C) was significantly higher in HBV carriers with LC compared to those without LC (LC; 86.1% vs non-LC; 72.1%, P=0.009). There was no difference in the genotype distribution of the IL-1RN polymorphism.

Conclusions: This is the first report describing the association between IL-1B polymorphism and HBV-related hepatic fibrosis, and our data suggest that IL-1B polymorphisms may be related to disease progression of HBV-related hepatitis in Japan.

MeSH terms

  • Adult
  • Aged
  • Disease Progression
  • Female
  • Genome, Viral / genetics
  • Hepatitis B / ethnology
  • Hepatitis B / etiology
  • Hepatitis B / genetics*
  • Hepatitis B / physiopathology
  • Hepatitis B virus / genetics*
  • Humans
  • Interleukin-1beta / genetics*
  • Japan
  • Liver Cirrhosis / etiology
  • Liver Cirrhosis / physiopathology
  • Liver Cirrhosis / virology
  • Male
  • Middle Aged
  • Polymorphism, Restriction Fragment Length*
  • Promoter Regions, Genetic / genetics
  • Promoter Regions, Genetic / physiology
  • Receptors, Interleukin-1 / antagonists & inhibitors
  • Receptors, Interleukin-1 / genetics
  • Risk Factors

Substances

  • Interleukin-1beta
  • Receptors, Interleukin-1