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
- 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
- NIDA NIH HHS [R01 DA024563, R01 DA024563-01] Funding Source: Medline
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.
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