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猪繁殖与呼吸综合征病毒(PRRSV)感染的抗体依赖性增强作用下调巨噬细胞中肿瘤坏死因子-α(TNF-α)和干扰素-β(IFN-β)的转录。

Antibody-dependent enhancement of PRRSV infection down-modulates TNF-α and IFN-β transcription in macrophages.

作者信息

Bao Dengke, Wang Rui, Qiao Songlin, Wan Bo, Wang Yinbiao, Liu Mingyang, Shi Xibao, Guo Juiqing, Zhang Gaiping

机构信息

College of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China; Key Laboratory of Animal Immunology of the Ministry of Agriculture, Henan Provincial Key Laboratory of Animal Immunology, Henan Academy of Agricultural Sciences, Zhengzhou 450002, China.

出版信息

Vet Immunol Immunopathol. 2013 Nov 15;156(1-2):128-34. doi: 10.1016/j.vetimm.2013.09.006. Epub 2013 Sep 19.

DOI:10.1016/j.vetimm.2013.09.006
PMID:24099951
Abstract

Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease, resulting in important economic losses in pig farming. Previous studies have shown that Fcγ receptor (FcγR)-mediated entry of infectious PRRSV immune complexes into macrophages plays a pivotal role in the pathogenesis of the disease. This study demonstrates that PRRSV was able to suppress the transcription of key antiviral genes tumor necrosis factor-α (TNF-α) and interferon-β (IFN-β), when infection was via the ADE pathway. Investigation of this infection pathway found that PRRSV suppresses the antiviral genes by disrupting the transcription of the genes coding for the associated transcription factors interferon regulatory factor-1 (IRF-1), interferon regulatory factor-3 (IRF-3) and nuclear factor kappa B (NF-κB). The ADE pathway of infection allows PRRSV to specifically target antiviral genes and alters the innate intracellular immune responses in macrophages. The ADE mechanism described in this study furthers our understanding of pathogenesis following PRRSV infection and is of general relevance to virally induced disease and in relation to antiviral vaccination strategies.

摘要

猪繁殖与呼吸综合征(PRRS)是一种传染病,给养猪业造成重大经济损失。先前的研究表明,Fcγ受体(FcγR)介导的传染性PRRSV免疫复合物进入巨噬细胞在该疾病的发病机制中起关键作用。本研究表明,当通过抗体依赖增强(ADE)途径感染时,PRRSV能够抑制关键抗病毒基因肿瘤坏死因子-α(TNF-α)和干扰素-β(IFN-β)的转录。对该感染途径的研究发现,PRRSV通过破坏编码相关转录因子干扰素调节因子-1(IRF-1)、干扰素调节因子-3(IRF-3)和核因子κB(NF-κB)的基因转录来抑制抗病毒基因。ADE感染途径使PRRSV能够特异性靶向抗病毒基因,并改变巨噬细胞内的固有免疫反应。本研究中描述的ADE机制进一步加深了我们对PRRSV感染后发病机制的理解,并且与病毒诱导的疾病以及抗病毒疫苗接种策略普遍相关。

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