Regulation and evasion of antiviral immune responses by porcine reproductive and respiratory syndrome virus

被引:82
作者
Huang, Chen [1 ,2 ]
Zhang, Qiong [1 ,2 ]
Feng, Wen-hai [1 ,2 ]
机构
[1] China Agr Univ, Coll Biol Sci, State Key Lab Agrobiotechnol, Beijing 100193, Peoples R China
[2] China Agr Univ, Coll Biol Sci, Dept Microbiol & Immunol, Beijing 100193, Peoples R China
基金
高等学校博士学科点专项科研基金;
关键词
PRRSV; Immune evasion; Type I IFNs; Apoptosis; Innate immunity; Adaptive immunity; NF-KAPPA-B; ANTIBODY-DEPENDENT ENHANCEMENT; PATTERN-RECOGNITION RECEPTORS; UNFOLDED PROTEIN RESPONSE; MODULATES TNF-ALPHA; T-CELL RESPONSES; DENDRITIC CELLS; NONSTRUCTURAL PROTEIN-2; PRRSV INFECTION; IN-VITRO;
D O I
10.1016/j.virusres.2014.12.014
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Virus infection of mammalian cells triggers host innate immune responses to restrict viral replication and induces adaptive immunity for viral elimination. In order to survive and propagate, viruses have evolved sophisticated mechanisms to subvert host defense system by encoding proteins that target key components of the immune signaling pathways. Porcine reproductive and respiratory syndrome virus (PRRSV), a RNA virus, impairs several processes of host immune responses including interfering with interferon production and signaling, modulating cytokine expression, manipulating apoptotic responses and regulating adaptive immunity. In this review, we highlight the molecular mechanisms of how PRRSV interferes with the different steps of initial antiviral host responses to establish persistent infection in pigs. Dissection of the PRRSV-host interaction is the key in understanding PRRSV pathogenesis and will provide a basis for the rational design of vaccines. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:101 / 111
页数:11
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