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Microb Pathog. 2016 Nov;100:84-89. doi: 10.1016/j.micpath.2016.09.001. Epub 2016 Sep 12.

Enterovirus 71 inhibits cellular type I interferon signaling by inhibiting host RIG-I ubiquitination.

Author information

1
College of Life Science and Technology, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China.
2
Department of Nephrology, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, 163319, China.
3
College of Life Science and Technology, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China; College of Animal Science and Veterinary Medicine, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China. Electronic address: cuiyudong@yahoo.com.
4
College of Life Science and Technology, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China; College of Animal Science and Veterinary Medicine, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China. Electronic address: 549076831@qq.com.
5
College of Life Science and Technology, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China; College of Animal Science and Veterinary Medicine, HeiLongJiang BaYi Agricultural University, Daqing, 163319, China. Electronic address: 673365630@qq.com.

Abstract

Enterovirus 71 (EV71) is a human pathogen that induces hand, foot, and mouth disease (HFMD) and fatal neurological diseases in young children and infants. Pathogenicity of EV71 is likely related to its ability to evade host innate immunity through inhibiting cellular type I interferon signaling. However, it is less well understood the molecular events governing this process. In this study, we found that EV71 infection suppressed the induction of antiviral immunity by inhibiting the expression levels of IFN-β and IFN-stimulated genes (ISGs), such as ISG54 and ISG56, at the late stage of viral infection. At the same time, our results showed that EV71 infection significantly inhibited ubiquitination of RIG-I. In contrast, up-regulation of RIG-I ubiquitination promoted expression of IFN-β and ISGs, suggesting that inhibition of cellular type I interferon signaling was caused by down-regulation of RIG-I ubiquitination during EV71 infection. These results suggest that inhibition of RIG-I-mediated type I IFN responses by EV71 may contribute to the pathogenesis of viral infection.

KEYWORDS:

Enterovirus 71; RIG-I; Type I interferon; Ubiquitination

PMID:
27633794
DOI:
10.1016/j.micpath.2016.09.001
[Indexed for MEDLINE]

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