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目的探讨乙型肝炎病毒(HBV)自限感染和慢性感染与原蛋白转化酶Furin P1启动区SNP-229C/T的关系。方法收集112例抗-HBs和抗-HBc阳性的HBV自限感染者和300例HBV慢性感染者的外周全血,提取基因组DNA;采用竞争分化聚合酶链反应技术为基础的方法对Furin P1启动区SNP-229 C/T进行基因分型。结果全部患者中,C等位基因频率为74.6%(615/824),T等位基因频率为25.4%(209/824),CC、CT和TT基因型的频率分别为60.9%(251/412)、27.4%(113/412)和11.7%(48/412),不完全符合Hardy-Weinberg分布。与自限感染相比,HBV慢性感染者携带较高频率的T等位基因(28.2%vs17.9%,P<0.01)、TT基因型(14.3%vs4.5%,P<0.01)和较低的C等位基因(71.8%vs82.1%,P<0.01)、CC基因型(58.0%vs68.8%,P<0.05)。在慢性感染患者中,HBeAg的状态与基因型分布无关。结论 Furin P1启动区SNP-229 C/T能在一定程度上影响HBV感染的转归,有望成为临床上HBV感染转归的预测指标。
Objective To investigate the relationship between self-limiting infection and chronic infection of hepatitis B virus (HBV) and the SNP-229C / T promoter in Furin P1 promoter. METHODS: Peripheral blood samples from 112 patients with HBV-positive and anti-HBc-positive HBV infection and 300 patients with chronic HBV infection were collected and genomic DNA was extracted. Furin P1 was initiated by competition-based polymerase chain reaction Region SNP-229 C / T for genotyping. Results The frequency of C allele was 74.6% (615/824), the frequency of T allele was 25.4% (209/824), the frequencies of CC, CT and TT genotypes were 60.9% (251/412 ), 27.4% (113/412) and 11.7% (48/412), respectively, which did not completely match the Hardy-Weinberg distribution. Patients with chronic HBV infection had higher frequency of T allele (28.2% vs17.9%, P <0.01), TT genotype (14.3% vs4.5%, P <0.01) Low C allele (71.8% vs82.1%, P <0.01), CC genotype (58.0% vs68.8%, P <0.05). In chronically infected patients, HBeAg status has nothing to do with genotype distribution. Conclusion The SNP-229 C / T of Furin P1 promoter region can affect the outcome of HBV infection to a certain extent, which is expected to become a predictor of clinical outcome of HBV infection.