A SNP in IFNGR1 promoter is correlated to the susceptibility to chronic HBV infection in Chinese population

Abstract

OBJECTIVES: The antiviral mechanism stimulated by interferon-gamma is found to be crucial for clearance of hepatitis B virus (HBV) in vivo. The antiviral signaling transduction is triggered by the specific binding between interferon-gamma and its receptor IFNGR1 (interferongamma receptor 1). Interferon-gamma signaling transduction pathway is directly controlled by the IFNGR1 expression level. In our study, single nucleotide polymorphisms (SNPs) in the IFNGR1 gene and the correlation between the SNPs and susceptibility to chronic HBV in Chinese were investigated. METHODS: Blood samples of 983 Chinese, including 361 chronic hepatitis B patients, 366 healthy individuals, and 256 hepatitis B spontaneously recovered patients, were collected. Seven SNPs (−611A/G, −56C/T, 40G/A, 95C/T, 130A/G, 20685A/G, 21227T/C) in IFNGR1 gene were identified by restriction fragment-length polymorphism (RFLP) assays. The transcription levels of different SNPs variants were compared by luciferase assays. RESULTS: −56C and −56T allele were found to be correlated to HBV clearance and persistence. In luciferase assays, the transcription level of IFNGR1 promoter with the −56C is significantly higher than that with −56T. CONCLUSION: −56C/T SNP in IFNGR1 promoter region is associated with susceptibility to chronic HBV in Chinese population.