INTERACTIONS BETWEEN THE HUMAN IMMUNODEFICIENCY VIRUS AND HERPESVIRUSES

我们一直在研究HSV和HIV基因之间的相互作用 分子水平。在第一个项目中，我们通过 哪种HSV-1能激活HIV RNA转录。单纯疱疹病毒的大量激活 依赖于HIV LTR中Sp1和NF-kB增强子的完整性。 单纯疱疹病毒还通过诱导一种细胞因子的表达来激活LTR 结合在HIV转录起始点附近的蛋白质。竞争 实验证明了该蛋白与紫外光交叉的结合特异性 相关研究发现了一种新的45kD蛋白。我们目前正在 试图提纯这种名为LBP-2的蛋白质。 在第二系列研究中，我们显示了HIV Tat的反式激活。 HSV-1潜伏期相关基因。瞬时表达分析显示 LAT启动子显著上调，而其他类型HSV-1无明显上调 推动者。LAT启动子序列的定点改变是 被用来定义那个纹身目标。

We have been studying the interactions between HSV and HIV genes at a molecular level. In the first project we are examining the mechanism by which HSV-1 activates HIV RNA transcription. The bulk of HSV activation is dependant on the integrity of Sp1 and NF-kB enhancers in the HIV LTR. HSV also activates the LTR by inducing the expression of a cellular protein that binds near the HIV transcriptional start site. Competition experiments proved the binding specificity of the protein and uV-cross linking studies identified a novel 45kD protein. We are currently attempting to purify the protein, termed LBP-2. In the second series of studies we showed that the HIV tat transactivates the HSV-1 latency-associated gene. Transient expression assays showed marked upregulation of LAT promoter but not other classes of HSV-1 promoters. Site-directed alterations in the LAT promoter sequence are being used to define that tat target.