The virus battles:: IFN induction of the antiviral state and mechanisms of viral evasion

被引:341
作者
Levy, DE
García-Sastre, A
机构
[1] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA
[2] NYU, Sch Med, Kaplan Comprehens Canc Ctr, New York, NY 10016 USA
[3] CUNY Mt Sinai Sch Med, Dept Microbiol, New York, NY 10029 USA
关键词
IFN; JAK; STAT; PKR; IRF; OAS;
D O I
10.1016/S1359-6101(00)00027-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Response to IFN involves a rapid and direct signal transduction mechanism that quickly reports that presence of extracellular cytokine to the cell nucleus, preserving the specificity inherent in cytokine-receptor interactions to transcriptionally induce expression of a set of genes encoding important antiviral proteins. Establishment of the resulting antiviral state provides a crucial initial line of defense against viral infection. Studies of IFN-deficient cells and animals derived by gene targeting have demonstrated the essential nature of IFN-mediated innate immunity. The long co-evolutionary history of viruses with their hosts as seen the development of a variety of evasive adaptions that allow viruses to circumvent or inactivate host antiviral mechanisms. Further understanding of both host and viral components of this battle may provide important new strategies for vaccine development and creation of novel antiviral compounds. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:143 / 156
页数:14
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