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首页> 外文期刊>Virology >Parainfluenza virus 5 upregulates CD55 expression to produce virions with enhanced resistance to complement-mediated neutralization
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Parainfluenza virus 5 upregulates CD55 expression to produce virions with enhanced resistance to complement-mediated neutralization

机译:Parainfluenza病毒5上调CD55表达以产生具有增强的抗性的病毒粒子,以补充介导的中和

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摘要

Many enveloped RNA viruses recruit host cell proteins during assembly as a mechanism to limit antiviral effects of complement. Using viruses which incorporated CD46 alone, CD55 alone or both CD46 and CD55, we addressed the role of these two host cell regulators in limiting complement-mediated neutralization of Parainfluenza virus 5 (PIV5). PIV5 incorporated functional forms of both CD55 and CD46 into virions. PIV5 containing CD55 was highly resistant to complement-mediated neutralization, whereas CD46-containing PIV5 was as sensitive to neutralization as virus lacking both regulators. PIV5 infected cells had increased levels of cell surface CD55, which was further upregulated by exogenous treatment with tumor necrosis factor alpha. PIV5 derived from cells with higher CD55 levels was more resistant to complement-mediated neutralization in vitro than virus from control cells. We propose a role for virus induction of host cell complement inhibitors in defining virus growth and tissue tropism. (C) 2016 Elsevier Inc. All rights reserved.
机译:许多包络RNA病毒在组装过程中募集宿主细胞蛋白作为限制补体的抗病毒影响的机制。使用单独掺入CD46的病毒,单独的CD55和CD46和CD55,我们解决了这两个宿主细胞调节剂在限制副血管病毒5(PIV5)的补体中和的作用。 PIV5将CD55和CD46的功能形式掺入病毒粒子中。 PIV5含CD55具有高度抗补体介导的中和的耐抗性,而CD46的PIV5与缺乏两个调节剂的病毒一样敏感。 PIV5感染的细胞具有增加的细胞表面CD55水平,其通过与肿瘤坏死因子α的外源治疗进一步上调。衍生自CD55水平较高的细胞的PIV5比来自对照细胞的病毒更抗CD55水平的细胞更耐受介导的中和。我们提出了在定义病毒生长和组织覆身宿主细胞补体抑制剂中的病毒诱导的作用。 (c)2016 Elsevier Inc.保留所有权利。

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