Suppression of interferon response gene expression in cells persistently infected with mumps virus, and restoration from its suppression by treatment with ribavirin

被引:29
作者
Fujii, N [1 ]
Yokosawa, N [1 ]
Shirakawa, S [1 ]
机构
[1] Sapporo Med Univ, Sch Med, Dept Microbiol, Chou Ku, Sapporo, Hokkaido 060, Japan
关键词
persistent infection; mumps virus; PKR; 2-5AS; MxA; HLA class-I; interferon; STAT-1; STAT-2; ISGF-3; gamma; ribavirin;
D O I
10.1016/S0168-1702(99)00114-8
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Persistent infections with mumps virus were established in human B-lymphoid cell line Akata and in the human chronic myelogenous leukaemia cell line K562. Even after IFN treatment a drastic decrease in STAT-1 alpha (signal transducers and activators of transcription-1 alpha) STAT-2 and p48 (ISGF-3 gamma: IFN-stimulated gene factor-3 gamma), which are closely correlated with the IFN-signaling pathway, was found in these persistently infected cells (Akata-MP1 and K-MTP). Therefore, the IFN-signaling pathway is thought to be defective in these persistently infected cells. In other words, most of the IFN-inducible genes in these cells persistently infected vith mumps virus may not be able to respond to IFN treatment. Indeed, pool induction of 2',5'-oligoadenylate synthetase (2-5AS), dsRNA activated protein kinase (PKR), and MxA protein mRNAs were demonstrated in these cell lines after IFN treatment. Expression of MHC class-I antigen was also significantly reduced in the persistently infected cell lines as compared with that of uninfected control cells. HLA antigen was augmented by IFN-alpha in Akata and K562 cells: but not in persistently infected cells. Furthermore, suppression of IFN-induced 2-5AS induction and MHC class-I expression was restored by treatment of persistently infected cells with ribavirin through inhibition of virus replication. The result of restoration was also confirmed by IFN-induced STAT-1 induction in persistently infected cells treated with ribavirin. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:175 / 185
页数:11
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