Modulation of the host toll-like receptor signaling pathways by virus infection.
- Author:
Zhi-Zhong JING
1
;
Xiao-Bing HE
;
Yong-Xiang FANG
;
Huai-Jie JIA
;
Tao ZHOU
Author Information
1. State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Public Health of Agricultural Ministry, Lanzhou Veterinary Research Institute, CAAS, Lanzhou 730046, China. zhizhongj@163.com
- Publication Type:Journal Article
- MeSH:
Animals;
Antiviral Agents;
pharmacology;
therapeutic use;
Humans;
Immunity, Innate;
drug effects;
Signal Transduction;
drug effects;
Toll-Like Receptors;
metabolism;
Virus Diseases;
drug therapy;
immunology;
metabolism;
pathology
- From:
Chinese Journal of Virology
2012;28(4):453-461
- CountryChina
- Language:Chinese
-
Abstract:
Toll-like receptors (TLRs) are germline-encoded pattern recognition receptors (PRRs) that play a central role in host cell recognition and responses to virus infection, leading to the production of interferons (IFNs) and proinflammatory cytokines. In parallel, in order to establish an infection, viruses have to develop exclusively strategies to interfere with TLRs signaling, particularly some important adaptors activation such as MyD88, NF-kappaB, TRIF and IRFs, and suppress or escape host's antiviral immune response. In this paper, we review the latest findings on the various strategies used by viruses to modulate TLRs-mediated innate immune response, with special emphasis on immune evasion mechanism of VACV, HCV and HIV. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses hamper TLRs signaling and how to overcome viral infection.
