Feng C P, Kulka M, Aurelian L
Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Baltimore 21201.
Virology. 1993 Feb;192(2):491-500. doi: 10.1006/viro.1993.1065.
Molecular interactions between the herpes simplex virus type 1 (HSV-1) and human immunodeficiency virus (HIV) were investigated in U937 cells. Nonpermissive HSV-1 infection of U937 cells activated HIV as determined in transient expression assays with hybrid constructions containing the HIV-LTR-directed chloramphenicol acetyltransferase gene. Activation was independent of kappa B-enhancer elements whereas these elements were required for HSV-1-mediated activation in another cell line (C6). kappa B-binding proteins were induced in U937 cells by HSV-1 infection. Four species (45, 55, 75, and 75/80 kDa) were identified by DNA-protein cross-linking. Methylation interference analysis defined close contact only with the third residue of the previously established critical contact triplet GGG. Transient expression assays using mutants in HIV-LTR revealed the presence a cis-response element (GGTCA palindrome) in the negative regulatory region.
在U937细胞中研究了单纯疱疹病毒1型（HSV-1）与人类免疫缺陷病毒（HIV）之间的分子相互作用。用含有HIV-LTR定向氯霉素乙酰转移酶基因的杂交构建体进行瞬时表达分析，结果表明，U937细胞对HSV-1的非允许性感染激活了HIV。激活不依赖于κB增强子元件，而在另一种细胞系（C6）中，这些元件是HSV-1介导的激活所必需的。HSV-1感染可诱导U937细胞中的κB结合蛋白。通过DNA-蛋白质交联鉴定出四种蛋白（45、55、75和75/80 kDa）。甲基化干扰分析表明，仅与先前确定的关键接触三联体GGG的第三个残基有紧密接触。使用HIV-LTR中的突变体进行的瞬时表达分析揭示了负调控区域中存在一个顺式反应元件（GGTCA回文序列）。
