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Characterization of the antiviral effects of interferon-α against a SARS-like coronoavirus infection in vitro

机译：干扰素-α对SARS样冠状病毒感染的体外抗病毒作用的表征

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Interferon (IFN)-αs bind to and activate their cognate cell surface receptor to invoke an antiviral response in target cells. Well-described receptor-mediated signaling events result in transcriptional regulation of IFN sensitive genes, effectors of this antiviral response. Results from a pilot study to evaluate the clinical efficacy of IFN-α treatment of SARS patients provided evidence for IFN-inducible resolution of disease. In this report we examined the contribution of IFN-inducible phosphorylation-activation of specific signaling effectors to protection from infection by a SARS-related murine coronavirus, MHV-1. As anticipated, the earliest receptor-activation event, Jak1 phosphorylation, is critical for IFN-inducible protection from MHV-1 infection. Additionally, we provide evidence for the contribution of two kinases, the MAP kinase p38MAPK, and protein kinase C (PKC) δ to antiviral protection from MHV-1 infection. Notably, our data suggest that MHV-1 infection, as for the Urbani SARS coronoavirus, inhibits an IFN response, inferred from the lack of activation of pkr and 2 '5 '-oas, genes associated with mediating the antiviral activities of IFN-αs. To identify potential target genes that are activated downstream of the IFN-inducible signaling effectors we identified, and that mediate protection from coronavirus infection, we examined the gene expression profiles in the peripheral blood mononuclear cells of SARS patients who received IFN treatment. A subset of differentially regulated genes were distinguished with functional properties associated with antimicrobial activities.
机译：干扰素（IFN）-α结合并激活其同源细胞表面受体，从而在靶细胞中引发抗病毒应答。充分描述的受体介导的信号转导事件导致IFN敏感基因（这种抗病毒应答的效应子）的转录调控。评估IFN-α治疗SARS患者临床疗效的前瞻性研究结果为IFN诱导的疾病解决提供了证据。在本报告中，我们研究了特定信号传导因子的IFN诱导的磷酸化激活对防止SARS相关鼠冠状病毒MHV-1感染的保护作用。如预期的那样，最早的受体激活事件Jak1磷酸化对于IFN诱导的MHV-1感染保护至关重要。此外，我们为MAP激酶p38MAPK和蛋白激酶C（PKC）δ这两种激酶对MHV-1感染的抗病毒保护做出了贡献。值得注意的是，我们的数据表明，与Urbani SARS冠状病毒一样，MHV-1感染抑制IFN反应，这是由于pkr和2'5'-oas缺乏激活所致，该基因与介导IFN-αs的抗病毒活性有关。为了鉴定潜在的靶基因，这些基因在我们确定的IFN诱导型信号转导子的下游被激活，并介导了对冠状病毒感染的保护，我们检查了接受IFN治疗的SARS患者外周血单核细胞中的基因表达谱。差异调节基因的一个子集具有与抗菌活性相关的功能特性。

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