Fujii N, Yokosawa N, Ishida S, Shirakawa S, Kubota T, Indoh T, Fujinaga K, Yashiki T
Department of Microbiology, Sapporo Medical University School of Medicine, Hokkaido, Japan.
Microbiol Immunol. 1996;40(10):777-81. doi: 10.1111/j.1348-0421.1996.tb01141.x.
Poor induction of interferon-induced 2', 5'-oligoadenylate synthetase (2-5AS) activity has been demonstrated in cells persistently infected with the mumps virus or human T-lymphotropic virus type-I (HTLV-I). The suppression of 2-5AS induction is the result of the repression of 2-5AS gene expression at the transcription level. In a general way, after the binding of interferon-alpha (IFN-alpha) to cell surface-specific receptors, expression of 2-5AS gene is thought to be regulated by some transacting factors, IFN-regulatory factors (IRF-1 and IRF-2) and the IFN-stimulated gene factor (ISGF-3, a complex consisting of STAT-1 alpha, STAT-2 and p48). To clarify the cause of the suppression mechanism(s), fluctuation in the number of IFN receptors and the levels of mRNAs in both IRF-1 and IRF-2 were examined in cells persistently infected with the mumps virus (FLMT and KBMT). There were few differences in the number of IFN receptors and the level of IRF-2 mRNA between persistently infected cells and uninfected control cells. After the treatment of cells with IFN, a slight reduction of IRF-1 mRNA was found in persistently infected cells as compared with that of the uninfected control cells.
在持续感染腮腺炎病毒或I型人类嗜T淋巴细胞病毒(HTLV-I)的细胞中,已证实干扰素诱导的2',5'-寡腺苷酸合成酶(2-5AS)活性诱导不佳。2-5AS诱导的抑制是2-5AS基因表达在转录水平受到抑制的结果。一般来说,在α干扰素(IFN-α)与细胞表面特异性受体结合后,2-5AS基因的表达被认为受一些反式作用因子、干扰素调节因子(IRF-1和IRF-2)以及干扰素刺激基因因子(ISGF-3,一种由STAT-1α、STAT-2和p48组成的复合物)调控。为了阐明抑制机制的原因,在持续感染腮腺炎病毒的细胞(FLMT和KBMT)中检测了IFN受体数量以及IRF-1和IRF-2的mRNA水平的波动。持续感染的细胞与未感染的对照细胞相比,IFN受体数量和IRF-2 mRNA水平几乎没有差异。在用IFN处理细胞后,与未感染的对照细胞相比,持续感染的细胞中发现IRF-1 mRNA略有减少。