Association of interferon-gamma induced protein 10 promoter polymorphisms with the disease progression of hepatitis B virus infection in Chinese Han population

PLoS One. 2013 Sep 4;8(9):e72799. doi: 10.1371/journal.pone.0072799. eCollection 2013.

Abstract

Background and aims: Interferon-gamma induced protein 10 (IP-10) was suggested to be involved in liver injury in viral hepatitis. This study aimed to investigate the impact of the single nucleotide polymorphisms (SNP) G-201A (rs1439490) in IP-10 gene on disease progression of hepatitis B virus (HBV) infection.

Methods: The -201 SNP in IP-10 promoter was genotyped from 577 patients with different illness categories and 275 health controls; In vitro IP-10 promoter activity was compared between haplotype GG and AA homozygotes using luciferase reporter system in HepG2 cells. In vivo expression of IP-10 was compared between patients with -201 AA genotype and GG genotype.

Results: The detected frequency of G-201A SNP was 17.8%, 25.3%, 26.6%, and 13.8% for patients with acute hepatitis B (AHB), patients with mild chronic hepatitis B (CHB-M), patients with severe chronic hepatitis B (CHB-S), and health controls, respectively. In vitro IP-10 promoter-driven luciferase activity in pGL3-Enhancer-201A transfected HepG2 cells was 1.43-fold higher than that in pGL3-Enhancer-201G transfected HepG2 cells (P<0.01). In vivo IP-10 transcriptional expression of peripheral blood mononuclear cells was 1.38-fold higher in patients with -201 AA genotype than in patients with -201 GG genotype (P<0.01).

Conclusion: G-201A in promoter region of IP-10 gene was associated with liver disease progression in patients with HBV infection through up-regulating IP-10 expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asian People / genetics
  • Chemokine CXCL10 / genetics*
  • Female
  • Genetic Predisposition to Disease
  • Hepatitis B / genetics*
  • Humans
  • Male
  • Polymorphism, Genetic / genetics*
  • Young Adult

Substances

  • CXCL10 protein, human
  • Chemokine CXCL10

Grants and funding

This work was supported by the National Natural Science Foundation of China (81271847), and National 12th Five-Year Special Grand Project for Infectious Diseases (2012ZX10002004-005, 2012ZX10004503). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.