Innate immune evasion by hepatitis C virus and West Nile virus

被引:20
|
作者
Keller, Brian C.
Johnson, Cynthia L.
Erickson, Andrea Kaup
Gale, Michael, Jr.
机构
[1] Univ Washington, Sch Med, Dept Immunol, Seattle, WA 98195 USA
[2] Univ Texas, SW Med Ctr, Dept Microbiol, Dallas, TX USA
关键词
LGP2; IPS-1; IRF-3; MAVS; RIG-1; interferon; JAK; STAT;
D O I
10.1016/j.cytogfr.2007.06.006
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
Antiviral immunity in mammals involves several levels of surveillance and effector actions by host factors to detect viral pathogens, trigger alpha/beta interferon production, and to mediate innate defenses within infected cells. Our studies have focused on understanding how these processes are regulated during infection by hepatitis C virus (HCV) and West Nile virus (WNV). Both viruses are members of the Flaviviridae and are human pathogens, but they each mediate a very different disease and course of infection. Our results demonstrate common and unique innate immune interactions of each virus that govern antiviral immunity and demonstrate the central role of alpha/beta interferon immune defenses in controlling the outcome of infection. (c) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:535 / 544
页数:10
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