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首页> 外文期刊>Virus Research: An International Journal of Molecular and Cellular Virology >Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-beta production via blocking IPS-1 and RIG-I
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Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-beta production via blocking IPS-1 and RIG-I

机译:猪急性腹泻综合征冠状病毒(SADS-COV)通过阻塞IPS-1和RIG-I拮抗干扰素-β产生

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摘要

Swine acute diarrhea syndrome coronavirus (SADS-CoV), a newly emerging enteric coronavirus, is considered to be associated with swine acute diarrhea syndrome (SADS) which has caused significantly economic losses to the porcine industry. Interactions between SADS-CoV and the host innate immune response is unclear yet. In this study, we used IPEC-J2 cells as a model to explore potential evasion strategies employed by SADS-CoV. Our results showed that SADS-CoV infection failed to induce IFN-beta production, and inhibited poly (I:C) and Sendai virus (SeV)-triggered IFN-beta expression. SADS-CoV also blocked poly (I:C)-induced phosphorylation and nuclear translocation of IRF-3 and NF-kappa B. Furthermore, SADS-CoV did not interfere with the activity of IFN-beta promoter stimulated by IRF3, TBK1 and IKK epsilon, but counteracted its activation induced by IPS-1 and RIG-I. Collectively, this study is the first investigation that shows interactions between SADS-CoV and the host innate immunity, which provides information of the molecular mechanisms underlying SASD-CoV infection.
机译:猪急性腹泻综合征冠状病毒(Sads-Cov)是一种新出现的肠道冠状病毒,被认为与猪急性腹泻综合征(悲伤)有关,这对猪工业产生了显着的经济损失。 SADS-COV之间的相互作用尚不清楚。在这项研究中,我们使用IPEC-J2细胞作为探索Sads-Cov雇用的潜在逃号的模型。我们的研究结果表明,SADS-COV感染未能诱导IFN-Beta生产,抑制聚(I:C)和仙台病毒(Sev) - 触发IFN-β表达。 SADS-COV也封闭聚(I:C) - 诱导的IRF-3和NF-Kappa B的磷酸化和核易位。此外,Sads-CoV不会干扰IRF3,TBK1和IKK刺激的IFN-β启动子的活性epsilon,但抵消了IPS-1和Rig-i引起的激活。集体,本研究是第一次显示SAS-COV与宿主先天免疫之间的相互作用,这提供了SASD-COV感染的分子机制的信息。

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