慢性乙型和丙型肝炎病毒感染与白细胞介素-4-589基因多态性的关系

Association of IL-4-589 Polymorphisms with Chronic Hepatitis B and Hepatitis C Virus Infection

目的研究慢性乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)感染与白细胞介素(IL)-4-589基因多态性(SNP)的关系,探讨其免疫遗传机制。方法对438名研究对象检测HBV、HCV感染标志物,筛选出健康对照者74例和感染者203例,其中HBV合并HCV感染组79例,单纯HBV感染组69例,HCV感染组55例。用Beckman LX-20全自动生化仪检测丙氨酸氨基转移酶(ALT),逆转录套式聚合酶链技术(RT-n-PCR)检测HCV-RNA表达,并分析IL-4-589 SNP,观察SNP与慢性HBV或HCV感染、HCV病毒复制和ALT的关系。结果 IL-4-589位点基因型和等位基因频率与感染类型和HCV-RNA复制均无关系(P>0.05);IL-4-589位点基因型和等位基因频率ALT≥80 U/L组与<80 U/L组比较差异有统计学意义(P<0.01);携带CT和CC基因型肝脏损伤的OR值是TT基因型的3.43和8.25倍;携带C等位基因的肝脏损伤的风险是T等位基因的2.31倍。结论 IL-4-589位点CT、CC基因型和C等位基因能增加HBV和(或)HCV感染者的肝脏炎性损伤。

Objective To study the relationship between the polymorphisms in interleukin4 gene at position-589 （IL-4- 589） and chronic HBV and （or） HCV infection, and to explore the mechanisms. Methods 438 subjects were recruited which included 74 healthy collators and 205 infected person, among that 79 cases with HCV-HBV co-infections, 69 cases with simple HBV infections and 55 cases with HCV infections. Alanine aminotransferase （ALT） were detected by Beckman LX-20 automatic biochemistry. The HCV-RNA expressions were detected by reverse transcription nested polymerase chain reaction （RT-n-PCR）. The genes polymorphisms of IL-4 at 589 were investigated. The relation among SNP, chronic HBV infection, HCV infection, HCV virus replication, and ALT were observed. Results IL-4-589 genotype and allele frequency showed no significant association with persistent HBV and （or） HCV infection; the polymorphisms of IL-4-589 showed no association with HCV-RNA replication （P 〉 0.05）. The polymorphisms of IL-4-589 were significantly associated with abnormal ALT （ALTo〉80 U/L group vs ALT 〈80 U/L group, P 〈0.01）. Abnormal serum ALT level was associated with IL4-589 CC and CT genotype compared to Tr with the OR of 8.25 and 3.43） ; the OR of abnormal serum ALT level associated with the C allele compared to T allele was 2.31. Conclusion IL-4-589 CT, CC genotype, and C allele are possible risks to induce hver inflammatory injury.