He Yingli, Zhao YingRen, Zhang Shulin, Chen Wei, Lin ShuMei, Yang Qian, Liu JinFeng, Yang Yuan, Jin Yan, Liu Ming
Department of Infectious Diseases, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China.
J Clin Virol. 2006 Dec;37(4):282-6. doi: 10.1016/j.jcv.2006.08.012. Epub 2006 Sep 25.
Class II transactivator (CIITA) is the major rate-limiting regulator for expression of class II major histocompability complex (MHC-II). Human CIITA gene expression is controlled by four distinct promoters (pIto pIV).
To evaluate the relationship among polymorphism and methylation status of CIITA gene promoters and persistent hepatitis B virus (HBV) infection.
We recruited 21 patients with hepatocellular carcinoma (HCC), 45 liver cirrhosis (LC), 65 chronic hepatitis B (CHB), 26 acute hepatitis B (AHB) and 95 healthy blood donors. Polymorphism of CIITA gene promoters was assayed by PCR-SSCP-sequencing. Bioinformatics analysis was employed to predict the existence of CpG islands. Methylation-specific PCR (MSP) was used to detect the methylation status of CIITA gene pIV.
No sequence differences were observed at CIITA genes pI, III and IV among HCC, LC, CHB, AHB patients and healthy controls. No CpG islands were found in the pI, pII and pIII sequences, but there was a CpG island in pIV. The frequency of methylated POV was not significantly different within persistent HBV infection groups (patients with HCC, LC or CHB). Significance was found between the persistent infection group and acute HBV infection or healthy controls.
CIITA gene promoter sequences are conserved. PIV is highly methylated and associated with host susceptibility to HBV persistent infection.
II类反式激活因子（CIITA）是II类主要组织相容性复合体（MHC-II）表达的主要限速调节因子。人类CIITA基因的表达受四个不同启动子（pI至pIV）控制。
评估CIITA基因启动子的多态性与甲基化状态和乙型肝炎病毒（HBV）持续感染之间的关系。
我们招募了21例肝细胞癌（HCC）患者、45例肝硬化（LC）患者、65例慢性乙型肝炎（CHB）患者、26例急性乙型肝炎（AHB）患者和95名健康献血者。通过PCR-SSCP测序分析CIITA基因启动子的多态性。采用生物信息学分析预测CpG岛的存在。甲基化特异性PCR（MSP）用于检测CIITA基因pIV的甲基化状态。
在HCC、LC、CHB、AHB患者和健康对照者中，CIITA基因的pI、III和IV未观察到序列差异。在pI、pII和pIII序列中未发现CpG岛，但在pIV中有一个CpG岛。在持续HBV感染组（HCC、LC或CHB患者）中，甲基化pIV的频率无显著差异。在持续感染组与急性HBV感染组或健康对照之间发现有显著差异。
CIITA基因启动子序列保守。pIV高度甲基化并与宿主对HBV持续感染的易感性相关。
