4.6 Review

Innate immune evasion by hepatitis C virus and West Nile virus

期刊

CYTOKINE & GROWTH FACTOR REVIEWS
卷 18, 期 5-6, 页码 535-544

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.cytogfr.2007.06.006

关键词

LGP2; IPS-1; IRF-3; MAVS; RIG-1; interferon; JAK; STAT

资金

  1. NIAID NIH HHS [R21 AI057568, U01 AI048235, R56 AI060389, R01 AI060389-08, R21 AI057568-01A2, AI060389, R01 AI060389, U19 AI040035, AI48235, AI040035, AI057568] Funding Source: Medline
  2. NIDA NIH HHS [R01 DA024563, R01 DA024563-01] Funding Source: Medline

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据