Young D F, Carlos T S, Hagmaier K, Fan L, Randall R E
School of Biology, University of St. Andrews, Fife KY16 9ST, Scotland, UK.
Virology. 2007 Aug 15;365(1):238-40. doi: 10.1016/j.virol.2007.03.061. Epub 2007 May 16.
Whilst screening various cell lines for their ability to respond to interferon (IFN), we noted that in comparison to other tissue culture cells AGS tumour cells, which are widely used in biomedical research, had very low levels of STAT1. Subsequent analysis showed that the reason for this is that AGS cells are persistently infected with parainfluenza virus type 5 (PIV5; formally known as SV5), a virus that blocks the interferon (IFN) response by targeting STAT1 for proteasome-mediated degradation. Virus protein expression in AGS is altered in comparison to the normal pattern of virus protein synthesis observed in acutely infected cells, suggesting that the AGS virus is defective. We discuss the relevance of these results in terms of the need to screen cell lines for persistent virus infections that can alter cellular functions.
在筛选各种细胞系对干扰素(IFN)的反应能力时,我们注意到,与其他用于生物医学研究的组织培养细胞相比,广泛应用于生物医学研究的AGS肿瘤细胞中STAT1水平非常低。随后的分析表明,其原因是AGS细胞持续感染了5型副流感病毒(PIV5;原称为SV5),该病毒通过靶向STAT1进行蛋白酶体介导的降解来阻断干扰素(IFN)反应。与急性感染细胞中观察到的正常病毒蛋白合成模式相比,AGS中的病毒蛋白表达发生了改变,这表明AGS病毒存在缺陷。我们根据筛选可能改变细胞功能的持续性病毒感染细胞系的必要性,讨论了这些结果的相关性。