Parainfluenza virus 5 upregulates CD55 expression to produce virions with enhanced resistance to complement-mediated neutralization.
Parainfluenza virus 5 upregulates CD55 expression to produce virions with enhanced resistance to complement-mediated neutralization.
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DOI：
10.1016/j.virol.2016.07.030
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发表时间：
2016-10
期刊：
影响因子：
3.7
通讯作者：
Parks GD
中科院分区：
文献类型：
--
作者：
Li Y;Johnson JB;Parks GD
许多包膜RNA病毒在组装过程中招募宿主细胞蛋白，作为限制补体抗病毒作用的机制。使用单独掺入CD46、单独掺入CD55或同时掺入CD46和CD55的病毒，我们探讨了这两种宿主细胞调节因子在限制补体介导的副流感病毒5型（PIV5）中和中的作用。PIV 5将CD55和CD46的功能形式并入病毒体中。含CD55的PIV 5对补体介导的中和具有高度抗性，而含CD46的PIV 5对中和的敏感性与缺乏这两种调节因子的病毒一样。PIV 5感染的细胞具有增加的细胞表面CD55水平，其通过用肿瘤坏死因子α进行外源性处理而进一步上调。与来自对照细胞的病毒相比，来自具有较高CD55水平的细胞的PIV 5对补体介导的体外中和更具抗性。我们提出了病毒诱导宿主细胞补体抑制剂在定义病毒生长和组织嗜性中的作用。
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.
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影响因子：
6
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