Genomics Inform.  2013 Mar;11(1):15-23. 10.5808/GI.2013.11.1.15.

Association between Interferon-Inducible Protein 6 (IFI6) Polymorphisms and Hepatitis B Virus Clearance

• Park GH
• Kim KY
• Cho SW
• Cheong JY
• Yu GI
• Shin DH
• Kwack KB

• KMID: 1806266
• DOI: http://doi.org/10.5808/GI.2013.11.1.15

Abstract

CD8+ T cells are key factors mediating hepatitis B virus (HBV) clearance. However, these cells are killed through HBV-induced apoptosis during the antigen-presenting period in HBV-induced chronic liver disease (CLD) patients. Interferon-inducible protein 6 (IFI6) delays type I interferon-induced apoptosis in cells. We hypothesized that single nucleotide polymorphisms (SNPs) in the IFI6 could affect the chronicity of CLD. The present study included a discovery stage, in which 195 CLD patients, including chronic hepatitis B (HEP) and cirrhosis patients and 107 spontaneous recovery (SR) controls, were analyzed. The genotype distributions of rs2808426 (C > T) and rs10902662 (C > T) were significantly different between the SR and HEP groups (odds ratio [OR], 6.60; 95% confidence interval [CI], 1.64 to 26.52, p = 0.008 for both SNPs) and between the SR and CLD groups (OR, 4.38; 95% CI, 1.25 to 15.26; p = 0.021 and OR, 4.12; 95% CI, 1.18 to 14.44; p = 0.027, respectively). The distribution of diplotypes that contained these SNPs was significantly different between the SR and HEP groups (OR, 6.58; 95% CI, 1.63 to 25.59; p = 0.008 and OR, 0.15; 95% CI, 0.04 to 0.61; p = 0.008, respectively) and between the SR and CLD groups (OR, 4.38; 95% CI, 1.25 to 15.26; p = 0.021 and OR, 4.12; 95% CI, 1.18 to 14.44; p = 0.027, respectively). We were unable to replicate the association shown by secondary enrolled samples. A large-scale validation study should be performed to confirm the association between IFI6 and HBV clearance.

Keyword

hepatitis B virus; IFI6; single nucleotide polymorphism

MeSH Terms

Apoptosis
Fibrosis
Genotype
Hepatitis
Hepatitis B
Hepatitis B virus
Hepatitis B, Chronic
Humans
Liver Diseases
Negotiating
Polymorphism, Single Nucleotide
T-Lymphocytes