Roulston A, Conti L, McKiel V, Wainberg M A, Hiscott J
Abe Stern Cancer Research Laboratory, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada.
Leukemia. 1994 Apr;8 Suppl 1:S170-4.
The correlation between virus induced NF-kappa B DNA binding activity and interferon gene expression was examined in the myelomonoblastic PLB-985 cell line. Previous studies have shown that chronic HIV-1 infection of PLB-985 cells (PLB-IIIB) leads to the selection of cells with a more differentiated monocytic phenotype and with constitutive NF-kappa B DNA-binding activity. In this report we demonstrate that the kinetics of HIV-1 and Sendai virus infection of PLB-985 cells directly correlates with induction of NF-kappa B DNA binding activity. Based on UV cross-linking and immunoprecipitation analysis, p50, the strong transcriptional activator p65 and c-Rel represent the major constituents of this NF-kappa B DNA-binding activity. We also demonstrate an alteration in the kinetics of type I IFN gene transcription following secondary Sendai virus infection of PLB-IIIB cells compared to PLB-985. The results of our studies suggest that HIV infected individuals may respond differently to secondary viral or bacterial infections by augmenting the synthesis of NF-kappa B regulated immune response modifiers, which could alter the onset or progression of AIDS.
在骨髓单核细胞性PLB - 985细胞系中检测了病毒诱导的核因子κB（NF-κB）DNA结合活性与干扰素基因表达之间的相关性。先前的研究表明，PLB - 985细胞（PLB-IIIB）的慢性HIV-1感染导致选择具有更分化单核细胞表型且具有组成性NF-κB DNA结合活性的细胞。在本报告中，我们证明PLB - 985细胞的HIV-1和仙台病毒感染动力学与NF-κB DNA结合活性的诱导直接相关。基于紫外线交联和免疫沉淀分析，p50、强转录激活因子p65和c-Rel代表了这种NF-κB DNA结合活性的主要成分。我们还证明，与PLB - 985相比，PLB-IIIB细胞在二次感染仙台病毒后I型干扰素基因转录动力学发生了改变。我们的研究结果表明，HIV感染个体可能通过增加NF-κB调节的免疫反应调节剂的合成，对二次病毒或细菌感染产生不同反应，这可能会改变艾滋病的发病或进展。
