Adachi A, Oshima Y, Koyama A H
Department of Virology, The University of Tokushima School of Medicine, Tokushima 770-8503, Japan.
Int J Mol Med. 1999 Mar;3(3):311-3. doi: 10.3892/ijmm.3.3.311.
To investigate whether vaccinia virus (VV) can augment gene expression of human immunodeficiency virus type 1 (HIV-1), co-transfection experiments were carried out in which recombinant plasmids containing various portions of the HIV-1 long terminal repeat (LTR) linked to the chloramphenicol acetyltransferase (CAT) gene were transfected into cultured cells. A high level of enhancement in CAT activity directed by the HIV-1 LTRs containing the enhancer sequence was observed in cells infected with VV, as in the cells infected with type 1 herpes simplex virus (HSV-1). The sequence responsible for this augmentation of CAT activity was different from that recognized by HIV-1 Tat. These data clearly demonstrated that VV transactivates HIV-1 LTR through a mechanism distinct from that of activation by HIV-1 Tat.
为研究痘苗病毒（VV）是否能增强1型人类免疫缺陷病毒（HIV-1）的基因表达，进行了共转染实验，将含有与氯霉素乙酰转移酶（CAT）基因相连的HIV-1长末端重复序列（LTR）各部分的重组质粒转染到培养细胞中。在感染VV的细胞中，观察到由含有增强子序列的HIV-1 LTRs指导的CAT活性有高水平增强，这与感染1型单纯疱疹病毒（HSV-1）的细胞情况相同。导致这种CAT活性增强的序列与HIV-1 Tat识别的序列不同。这些数据清楚地表明，VV通过一种不同于HIV-1 Tat激活的机制反式激活HIV-1 LTR。
