Díaz-Guerra M, Rivas C, Esteban M
Centro Nacional de Biotecnología, CSIC, Madrid, Spain.
Virology. 1997 Sep 29;236(2):354-63. doi: 10.1006/viro.1997.8719.
The interferon (IFN)-induced enzyme RNase L produced by a recombinant vaccinia virus (VV) causes death of mammalian cells with morphological and biochemical characteristics of apoptosis. Coexpression of 2-5A-synthetase enhances apoptosis induced by RNase L Activation of endogenous RNase L by infection with a VV ts mutant (ts22) or with wild-type virus in the presence of the antipoxvirus drug isatin-beta-thiosemicarbazone, a treatment known to significantly increase the amount of double-stranded RNA late during infection, also causes pronounced apoptosis of infected cells. The effects observed with recombinant virus-derived RNase L or with the endogenous enzyme are specific, since apoptosis also occurs in cells derived from mice lacking the IFN-induced protein kinase (PKR). The apoptosis antagonist Bcl-2 prevents induction of cell death by RNase L activation. Apoptosis of mammalian cells by RNase L activation could be a mechanism mediating anticellular actions of IFN.
由重组痘苗病毒（VV）产生的干扰素（IFN）诱导酶核糖核酸酶L会导致哺乳动物细胞死亡，其具有凋亡的形态学和生化特征。2-5A合成酶的共表达增强了核糖核酸酶L诱导的凋亡。用痘苗病毒ts突变体（ts22）感染或在抗痘病毒药物异烟肼-β-硫代半卡巴腙存在下用野生型病毒感染激活内源性核糖核酸酶L，已知这种处理会在感染后期显著增加双链RNA的量，这也会导致被感染细胞明显凋亡。用重组病毒衍生的核糖核酸酶L或内源性酶观察到的效应是特异性的，因为在缺乏IFN诱导蛋白激酶（PKR）的小鼠来源的细胞中也会发生凋亡。凋亡拮抗剂Bcl-2可防止核糖核酸酶L激活诱导细胞死亡。核糖核酸酶L激活诱导哺乳动物细胞凋亡可能是介导IFN抗细胞作用的一种机制。
