原蛋白转化酶FurinP1启动区SNP一229C／T影响HBV感染的转归

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FurinP1启动区SNP一229C／T的关系。方法收集112例抗一HBs和抗一HBe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FurinP1启动区SNP一229C／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）、1Tr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FurinP1启动区SNP．229C／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。

The Single Nucleotide Polymorphism-229 C/T in the P1 Promoter of the Furin Gene Influences the Outcomes of HBV Infection

Objective To explore the relationship between a single nucleotide polymorphism-229.C/T in the P1 promoter of the Furin gene and the self-limited or chronic infection of HBV. Methods Peripheral blood samples from 112 adult subjects with self-limited HBV infection（ positive for both anti-HBs and anti-HBe） and 300 adult patients with chronic HBV infection were collected. A single nucleotide polymorphism-229 C/T in the P1 promoter of the Furin gene was typed using a protocol based on competitively differentiated-polymerase chain reaction. Results In all patients,the C and T allele frequencies were 74.6% （615/ 824 ） and 25.4% （ 209/824）, respectively CC, CT and TF genotype frequencies were 60.9% （ 251/412 ） ,27.4% （113/412） and 11.7% （48/412）. Tile genotype distribution didn＇ t completely follow Hardy-Weinberg equilibrium. Compared with the self-limited infection,the distribution frequencies of T allele（28.2% vs 17.9% ,P 〈0.01 ） and TT genotype（ 14.3% vs 4.5% ,P 〈 0. 01 ） were significantly higher, and oppositely, the those of C allele （71.8% vs 82.1% ,P 〈 0.01 ） and CC genotype（58.0% vs 68.8%, P 〈 0. 05 ） were significantly lower in chronic HBV infection. In patients with chronic infection, HBeAg status had no correlation to the distribution of genotypes. Conclusion The single nucleotide polymorphism-229 C/T in the P1 promoter of the Furin gene influenced the natural outcomes of HBV infection to some extent. This SNP may be used as a clinical prognostic marker of HBV infection.