title: [Association of interleukin-12 gene polymorphism with persistence of hepatitis B virus infection and hepatocellular carcinoma].
abstract: OBJECTIVE
  Infection with hepatitis B virus (HBV) may result in various conditions. Natural course of HBV infection is influenced by various host immune factors and cytokines play a crucial role in host immune defense. This study was undertaken to investigate the association between HBV persistence and development of hepatocelluar carcinoma (HCC) and single nucleotide polymorphisms (SNPs) of interleukin (IL)-12A.
  
  
  METHODS
  Between March 2002 and December 2004, seven hundred thirty Korean patients with HBV infection and 320 healthy individuals who recovered from HBV infection were enrolled. We assessed polymorphisms and haplotype in IL-12A, and the genotype distributions of the HBV clearance and persistence groups were compared in order to investigate the association between HBV persistence and SNPs of IL-12A. Moreover, the genotypic distributions between patients with HCC and without HCC were compared to investigate the association between the development of HCC and SNPs of IL-12A.
  
  
  RESULTS
  We asssesed the SNPs of IL-12A at position +6400, +6624 and +7003. On the basis of logistic regression analysis, no statistically significant association with HBV persistence was observed with IL-12A exon 7 +6400, +6624, 3' UTR +7003 SNP and haplotype of IL-12A +6400/+6624/+7003. Furthermore, no statistically significant association of HCC development with IL-12A exon 7 +6400, +6624, 3' UTR +7003 SNP and haplotype of IL-12A +6400/+6624/+7003 was observed.
  
  
  CONCLUSIONS
  These results suggest that SNPs and haplotype of IL-12A are not associated with HBV persistence and development of HCC. Further studies are needed to identify the host genetic factors in immune defense including cytokine gene polymorphisms of both IL-12A and IL-12B.
authors.affiliation: Department of Gastroenterology, Genomic Research Center for Gastroenterology, Ajou University School of Medicine, Suwon, Korea.
authors.forename: Jin Sun
authors.initials: JS
authors.lastname: Park
authors.forename: Jae Youn
authors.initials: JY
authors.lastname: Cheong
authors.forename: Joon Koo
authors.initials: JK
authors.lastname: Kang
authors.forename: Jin Hee
authors.initials: JH
authors.lastname: Cho
authors.forename: Sukyong
authors.initials: S
authors.lastname: Yu
authors.forename: Hyoung Doo
authors.initials: HD
authors.lastname: Shin
authors.forename: Byung Lae
authors.initials: BL
authors.lastname: Park
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Cho
mesh_terms: D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000209:etiology / Q000235:genetics* / Q000821:virology; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes; D006509:Hepatitis B / Q000150:complications / Q000235:genetics*; D006515:Hepatitis B virus / Q000302:isolation & purification; D019694:Hepatitis B, Chronic / Q000150:complications / Q000235:genetics*; D006579:Heterozygote; D006801:Humans; D053765:Interleukin-12 Subunit p35 / Q000235:genetics*; D008113:Liver Neoplasms / Q000209:etiology / Q000235:genetics* / Q000821:virology; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012189:Retrospective Studies; D012307:Risk Factors
chemical_list: D053765:Interleukin-12 Subunit p35