摘要
目的探讨肿瘤坏死因子α(TNF-α)和维生素D受体(VDR)基因多态位点交互作用与2型肝炎病毒(HBV)感染慢性化的关系。方法391例慢性乙型肝炎(CHB)患者为病例组和212例乙型肝炎病毒自限性感染者为对照组,应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测TNF-α基因启动子区-238G/A、-857C/T、-863C/A、VDR-TaqⅠT/C和FokⅠC/T位点的基因型,采用相乘模型分析基因-基因间的交互作用。结果TNF-α-238GA与VDR-FokⅠCT/CC(ORint=4.04)、TNF-α-863 CC与-857 CC(ORint=1.26)、VDR-FokⅠCT/CC与TNF-α-857 CC的基因间(ORint=1.37)均为正交互作用,增加HBV感染发展为慢性乙型肝炎的风险;TNF-α-238 GA与-857 CC(ORint=0.92)、VDR-FokⅠCT/CC与TNF-α-863 CC基因间(ORint=0.95)为负交互作用,降低HBV感染发展为慢性乙型肝炎的风险。结论TNF-α和VDR基因间交互作用可能影响HBV感染结局。
Objective To determine potential gene-gene interactions of TNF-α and VDR loci with outcomes of hepatitis B virus （HBV） infection. Methods A total of 391 chronic hepatitis B （HB） patients as a case group and 212 HBV self-limited infected subjects as a control group were recruited to conduct a case-control study. TNF-α - 238G/A, -857C/T, -863C/A, VDR-Taq Ⅰ T/C and Fok Ⅰ C/T gene polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP）. The interactions between TNF-α and VDR genes were analyzed by multiple model. Results There were positive gene-gene interactions between TNF-α -238 GA and Fok Ⅰ CT/CC（ORint =4. 04）,between -863 CC and -857 CC（ ORint = 1.26） and between -857 CC and Fok Ⅰ CT/CC（ ORint = 1.37 ）, respectively ,which increase the risk of chronic hepatitis B. There were negative gene-gene interactions between TNF-α - 238 GA and - 857 CC （ ORint = 0. 92 ） and between Fok Ⅰ CT/CC and TNF-α -863 CC（ ORint = 0. 95 ）, which decrease the risk of chronic hepatitis B. Conclusion Interaction between TNF-α loci and VDR loci potentially increase the risk of chronic hepatitis B after HBV infection.
出处
《基础医学与临床》
CSCD
北大核心
2008年第7期729-733,共5页
Basic and Clinical Medicine
基金
北京市科委重大项目(H020920020590)
