M. Salehi, Mohebbi, M. Karkhane, Shabnam Kazemian, P. Azimzadeh, M. S. Niasar, A. Sharifian, Zali
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引用次数: 0
摘要
背景与目的:白细胞介素18是一种细胞因子,通过与白细胞介素12 (IL-18)协同诱导干扰素γ活性,在th1介导的免疫应答中发挥重要作用。白细胞介素12和白细胞介素18在病毒纯化中起重要作用。考虑到IL-18的重要性,本研究探讨白细胞介素-18基因多态性(-607 C/A: rs1946518)与慢性乙型肝炎感染易感性的关系。方法:采用盐析法提取115例慢性乙型肝炎患者(HBsAg和Anti-HBcAb血清学检测结果阳性)和115例非hbv感染对照(HBsAg和AntiHbcAb血清学检测结果阴性,无肝病史)的基因组DNA,采用PCR-RFLP法测序单核苷酸多态性基因型(-607 C / A: rs1946518)。发现:患者中TT、GT和GG基因型频率分别为40%、49.6%和10.4%,对照组中分别为41.7%、42.6%和15.7%。患者组与对照组无明显差异。结论:基于本研究的结果,IL-18多态性与慢性乙型肝炎感染的可能性之间没有明确的关系。因此,这种多态性不可能是慢性乙型肝炎的潜在因素。
Lack of Genetic Association between Interleukin-18 Gene Polymorphism (rs1946518) and Chronic Hepatitis B Infection
BACKGROUND AND OBJECTIVE: Interleukin 18 is a member of the cytokines that play an important role in the Th1-mediated immune response by inducing interferon-gamma activity in collaboration with Interleukin-12 (IL-18). Interleukin 12 and Interleukin 18 can play an important role in purifying viruses. Considering the importance of IL-18, this study was conducted to investigate the relationship between Interleukin-18 Gene polymorphism (-607 C/A: rs1946518) and the susceptibility to chronic hepatitis B infection. METHODS: In this case-control study, the genomic DNA of 115 patients with chronic hepatitis B (with positive results of HBsAg and Anti-HBcAb serology testing) and 115 non-HBV-infected controls (negative results of HBsAg and AntiHbcAb serology testing and no history of liver disease) was extracted by salting-out method and the genotype of singlenucleotide polymorphism (-607 C / A: rs1946518) was sequenced using PCR-RFLP method. FINDING: The genotype frequency of TT, GT, and GG in patients was 40%, 49.6%, and 10.4% in patients, and 41.7%, 42.6%, and 15.7% in the control group, respectively. No significant difference was found between the patients group and the control group. CONCLUSION: Based on the results of this study, there was no clear relationship between IL-18 polymorphism and the potential for chronic hepatitis B infection. Therefore, this polymorphism cannot be a potential factor for chronic hepatitis B.