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PRV-encoded UL13 protein kinase acts as an antagonist of innate immunity by targeting IRF3-signaling pathways
Veterinary Microbiology ( IF 3.3 ) Pub Date : 2020-09-28 , DOI: 10.1016/j.vetmic.2020.108860
Lin Lv 1 , Mingzhu Cao 1 , Juan Bai 1 , Ling Jin 2 , Xianwei Wang 1 , Yanni Gao 1 , Xuewei Liu 1 , Ping Jiang 3
Affiliation  

Pseudorabies virus (PRV), a porcine alphaherpesvirus, causes neurological disorders and reproductive failure in swine. It is capable of avoiding host antiviral responses, resulting in viral latency in infected animals. The mechanisms by which many PRV proteins help the virus to evade immune surveillance are poorly understood. In this study, we found that the PRV protein kinase, UL13, inhibits the IFN-β signaling pathway by targeting interferon regulatory factor 3 (IRF3) for ubiquitination and degradation. PRV with mutant of UL13 is impaired in its ability to hinder IRF3 and interferon-β (IFN-β) activation, and has significantly less pathogenesis in mice that wild-type PRV. Our findings reveal an as yet undescribed mechanism utilized by PRV to evade host immune responses. PRV UL13 is a potential target for attenuated vaccines and antiviral drugs.



中文翻译:

PRV编码的UL13蛋白激酶通过靶向IRF3信号通路充当先天免疫的拮抗剂

伪狂犬病病毒(PRV)是一种猪α疱疹病毒,会引起猪的神经系统疾病和生殖衰竭。它能够避免宿主抗病毒反应,从而导致被感染动物的病毒潜伏期。许多PRV蛋白帮助病毒逃避免疫监视的机制了解甚少。在这项研究中,我们发现PRV蛋白激酶UL13通过靶向干扰素调节因子3(IRF3)的泛素化和降解来抑制IFN-β信号传导途径。具有UL13突变体的PRV阻碍IRF3和干扰素-β(IFN-β)活化的能力受损,并且在小鼠中的发病机理远低于野生型PRV。我们的发现揭示了PRV用来逃避宿主免疫反应的一种尚未描述的机制。PRV UL13是减毒疫苗和抗病毒药物的潜在靶标。

更新日期:2020-10-11
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