中文摘要：

为分析JDV与BIV、HIV-1 LTR和Tat相互激活能力差异的原因，在氨基酸序列对比及HIV-1 Tat功能域划分的基础上构建了JH、HJ、JB、BJ几种嵌合Tat蛋白，并克隆到真核表达载体。将上述表达质粒与以JDV、BIV和HIV-1 LTR为启动子，以觑c为报告基因的质粒共转染Hela细胞，证实了三种不同Tat激活能力的差异主要来自其结合域RNA结合能力的差异，排除了结构域不完整和细胞因子缺乏造成Ⅲ不激活HIV-1 LTR的可能性。

英文摘要：

In order to find the cause of different transactivate abilities among JDV, BIV and HIV-1 Tat, four chimeric Tat cDNA expression constructs, JH, HJ, JB and B J, were generated with the crossover points at the boundary of activation and binding domains based on functional domain division of HIV- 1 Tat and amino acid sequence comparision among HIV-1, JDV and BIV Tat. These chimeric Tat proteins were co-transfected with JDV, BIV and HIV-1 LTR report plasmids in Hela. Transient assay showed that different transactivate abilities among JDV, BIV and HIV-1 Tat were mainly caused by different binding abilities of their binding domains. We further excluded some possibilities that may cause the poor transactivate ability of JH on HIV-1 LTR, such as incomplete functional domains and the lack of related cytokines.