当前位置: X-MOL 学术J. Infect. Dis. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Control of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88).
The Journal of Infectious Diseases ( IF 6.4 ) Pub Date : 2020-05-11 , DOI: 10.1093/infdis/jiz602
Mathieu Iampietro 1 , Noemie Aurine 1 , Kevin P Dhondt 1 , Claire Dumont 1 , Rodolphe Pelissier 1 , Julia Spanier 2 , Audrey Vallve 3 , Herve Raoul 3 , Ulrich Kalinke 2, 4 , Branka Horvat 1
Affiliation  

Interferon (IFN) type I plays a critical role in the protection of mice from lethal Nipah virus (NiV) infection, but mechanisms responsible for IFN-I induction remain unknown. In the current study, we demonstrated the critical role of the mitochondrial antiviral signaling protein signaling pathway in IFN-I production and NiV replication in murine embryonic fibroblasts in vitro, and the redundant but essential roles of both mitochondrial antiviral signaling protein and myeloid differentiation primary response 88 adaptors, but not toll/interleukin-1 receptor/resistance [TIR] domain-containing adaptor-inducing IFN-β (TRIF), in the control of NiV infection in mice. These results reveal potential novel targets for antiviral intervention and help in understanding NiV immunopathogenesis.

中文翻译:

通过宿主适配器线粒体抗病毒信号蛋白(MAVS)和髓样分化主要反应88(MyD88)控制小鼠Nipah病毒感染。

I型干扰素(IFN)在保护小鼠免受致命性尼帕病毒(NiV)感染方面起着至关重要的作用,但是导致IFN-1诱导的机制仍然未知。在当前的研究中,我们证明了线粒体抗病毒信号蛋白信号转导通路在小鼠胚胎成纤维细胞中干扰素I产生和NiV复制中的关键作用,以及线粒体抗病毒信号蛋白和髓系分化主要反应的冗余但必不可少的作用在小鼠NiV感染的控制中,有88个衔接子,但没有收费/白介素1受体/抗性[TIR]域的诱导衔接子的IFN-β(TRIF)。这些结果揭示了抗病毒干预的潜在新目标,并有助于了解NiV免疫发病机制。
更新日期:2019-12-19
down
wechat
bug