共 68 条
Interferon-stimulated genes and their antiviral effector functions
被引:1019
作者:

Schoggins, John W.
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h-index: 0
机构:
Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, New York, NY 10065 USA Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, New York, NY 10065 USA

Rice, Charles M.
论文数: 0 引用数: 0
h-index: 0
机构:
Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, New York, NY 10065 USA Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, New York, NY 10065 USA
机构:
[1] Rockefeller Univ, Ctr Study Hepatitis C, Lab Virol & Infect Dis, New York, NY 10065 USA
关键词:
WEST-NILE-VIRUS;
RIG-I;
PROTEIN VIPERIN;
TRANSCRIPTION FACTOR;
STRANDED RNA;
IDENTIFICATION;
INHIBIT;
REPLICATION;
INDUCTION;
ALPHA;
D O I:
10.1016/j.coviro.2011.10.008
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
Many viruses trigger the type I interferon (IFN) system, leading to the transcription of hundreds of interferon-stimulated genes (ISGs). The products of these ISGs exert numerous antiviral effector functions, many of which are still not fully described. Recent efforts have been aimed at identifying which ISGs are antiviral and further characterizing their mechanisms of action. IFN effectors vary widely in their magnitude of inhibitory activity and display combinatorial antiviral properties. Collectively, ISGs can target almost any step in a virus life cycle. Some of the most potent antiviral effectors reinforce the system by further inducing IFN or ISGs. Other genes enhance or facilitate viral replication, suggesting that some viruses may have evolved to co-opt IFN effectors for a survival advantage.
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收藏
页码:519 / 525
页数:7
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