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轮状病毒对固有免疫反应的拮抗作用。

Rotavirus antagonism of the innate immune response.

机构信息

Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 50 South Drive MSC 8026, Room 6314, Bethesda, MD 20892-8026, USA; E-Mail:

出版信息

Viruses. 2009 Dec;1(3):1035-56. doi: 10.3390/v1031035. Epub 2009 Nov 24.

Abstract

Rotavirus is a primary cause of severe dehydrating gastroenteritis in infants and young children. The virus is sensitive to the antiviral effects triggered by the interferon (IFN)-signaling pathway, an important component of the host cell innate immune response. To counteract these effects, rotavirus encodes a nonstructural protein (NSP1) that induces the degradation of proteins involved in regulating IFN expression, such as members of the IFN regulatory factor (IRF) family. In some instances, NSP1 also subverts IFN expression by causing the degradation of a component of the E3 ubiquitin ligase complex responsible for activating NF-κB. By antagonizing multiple components of the IFN-induction pathway, NSP1 aids viral spread and contributes to rotavirus pathogenesis.

摘要

轮状病毒是导致婴幼儿严重腹泻脱水的主要原因。该病毒对干扰素(IFN)信号通路触发的抗病毒作用敏感,IFN 信号通路是宿主细胞固有免疫反应的重要组成部分。为了对抗这些作用,轮状病毒编码一种非结构蛋白(NSP1),该蛋白诱导调节 IFN 表达的蛋白降解,如 IFN 调节因子(IRF)家族的成员。在某些情况下,NSP1 还通过降解负责激活 NF-κB 的 E3 泛素连接酶复合物的一个成分来颠覆 IFN 表达。通过拮抗 IFN 诱导途径的多个成分,NSP1 有助于病毒传播并促进轮状病毒发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/3185539/3a5bb98ae5b9/viruses-01-01035f1.jpg

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