NDLI: Rotavirus nonstructural protein 1 antagonizes innate immune response by interacting with retinoic acid inducible gene I

Content Provider	Springer Nature : BioMed Central
Author	Qin, Lan Ren, Lili Zhou, Zhuo Lei, Xiaobo Chen, Lan Xue, Qinghua Liu, Xinlei Wang, Jianwei Hung, Tao
Abstract	Background The nonstructural protein 1 (NSP1) of rotavirus has been reported to block interferon (IFN) signaling by mediating proteasome-dependent degradation of IFN-regulatory factors (IRFs) and (or) the β-transducin repeat containing protein (β-TrCP). However, in addition to these targets, NSP1 may subvert innate immune responses via other mechanisms. Results The NSP1 of rotavirus OSU strain as well as the IRF3 binding domain truncated NSP1 of rotavirus SA11 strain are unable to degrade IRFs, but can still inhibit host IFN response, indicating that NSP1 may target alternative host factor(s) other than IRFs. Overexpression of NSP1 can block IFN-β promoter activation induced by the retinoic acid inducible gene I (RIG-I), but does not inhibit IFN-β activation induced by the mitochondrial antiviral-signaling protein (MAVS), indicating that NSP1 may target RIG-I. Immunoprecipitation experiments show that NSP1 interacts with RIG-I independent of IRF3 binding domain. In addition, NSP1 induces down-regulation of RIG-I in a proteasome-independent way. Conclusions Our findings demonstrate that inhibition of RIG-I mediated type I IFN responses by NSP1 may contribute to the immune evasion of rotavirus.
Related Links	https://virologyj.biomedcentral.com/counter/pdf/10.1186/1743-422X-8-526.pdf
Ending Page	9
Page Count	9
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/1743-422X-8-526
Journal	Virology Journal
Issue Number	1
Volume Number	8
Language	English
Publisher	BioMed Central
Publisher Date	2011-12-08
Access Restriction	Open
Subject Keyword	Virology Rotavirus Nonstructural protein 1 Interferon Retinoic acid inducible gene I
Content Type	Text
Resource Type	Article
Subject	Virology Infectious Diseases
Journal Impact Factor	4/2023
5-Year Journal Impact Factor	3.8/2023

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