School of Veterinary Medicine and Biomedical Sciences and the Nebraska Center for Virology, University of Nebraska-Lincoln, Lincoln, Nebraska 68583-0900, USA.
J Virol. 2010 May;84(9):4826-31. doi: 10.1128/JVI.02701-09. Epub 2010 Feb 24.
We show here that replication of defective interfering (DI) particle RNA in HEK293 cells stably expressing vesicular stomatitis virus (VSV) replication proteins potently activates interferon (IFN) and IFN signaling pathways through upregulation of IFN-beta promoter, IFN-stimulated response element (ISRE) promoter, and NF-kappaB promoter activities. Replication of DI particle RNA, not mere expression of the viral replication proteins, was found to be critical for induction of IFN and IFN signaling. The stable cells supporting replication of DI RNA described in this report will be useful in further examining the innate immune signaling pathways and the host cell functions in viral genome replication.
我们在此表明，在稳定表达水疱性口炎病毒（VSV）复制蛋白的 HEK293 细胞中，缺陷干扰（DI）颗粒 RNA 的复制能够通过上调 IFN-β启动子、IFN 刺激反应元件（ISRE）启动子和 NF-κB 启动子活性，强烈激活干扰素（IFN）和 IFN 信号通路。我们发现，DI 颗粒 RNA 的复制，而不仅仅是病毒复制蛋白的表达，对于诱导 IFN 和 IFN 信号至关重要。本报告中描述的支持 DI RNA 复制的稳定细胞将有助于进一步研究先天免疫信号通路和宿主细胞在病毒基因组复制中的功能。
