HIV-1感染对T和B细胞核内UNG2 mRNA表达的影响  

Up-regulation of human nuclear form of uracil-DNA glycosylase mRNA in HIV-1 infected human peripheral T cells and C8166 cells

作　　者：张驰宇[1] 许燕萍[1] 贲昆龙[2] 

机构地区：[1]江苏大学医学技术学院,江苏镇江212013 [2]中国科学院昆明动物研究所,云南昆明650223

出　　处：《江苏大学学报（医学版）》2007年第1期5-8,共4页Journal of Jiangsu University：Medicine Edition

基　　金：江苏省高校自然科学指导性计划资助项目(04KJD180044);江苏大学高级技术人才科研启动基金资助项目(2281270002)

摘　　要：目的:探讨HIV-1感染是否影响细胞中UNG2的表达。方法:采用四步法SYBR greenⅠ实时定量RT-PCR,对HIV-1感染者的T和B淋巴细胞,以及HIV-1感染的C8166细胞核内UNG2 mRNA的表达进行测定。结果:UNG2 mRNA的表达在HIV-1感染者的T细胞和HIV-1感染的C8166细胞中被明显上调,分别是对照的8.76倍和8.14倍,而在HIV-1感染者的B细胞中却没有被上调。结论:HIV-1感染导致的UNG2表达上调,可能通过减少TCR的多样性削弱Th的功能,另一方面可能有利于病毒对UNG2的包装。Objective： To investigate whether HIV-1 infection may activate the expression of nuclear UNG2 mRNA of T and B cells, which may inhibit antibody gene hypermutation and decrease antibody di- versity. Methods： The 4-step program in SYBR green I real-time RT-PCR was used to quantify the expression of UNG2 mRNA in T and B cells of HIV-l-infeeted individuals, and in HIV-1-infeeted C8166 cells. Results： The expression of UNG2 mRNA in T cells from HIV-1 infected patients and in C8166 cells infected with HIV-1 was found to be obviously up-regulated. Their relative expression indices were 8.76 and 8.14 in comparison with those of uninfected controls, respectively. Conclusion： The increased UNG2 in HIV-1 infected cells may lead to weakening Th cell function by decreasing TCR diversity, and may benefit incorporation of this enzyme into HIV-1 particles.

关 键 词：尿嘧啶DNA糖苷酶 HIV-1 T细胞受体 免疫逃逸 超突变 

分 类 号：Q5[生物学—生物化学] R512.91[医药卫生—内科学]