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Open AccessArticle

EV71 Infection Induces IFNβ Expression in Neural Cells

by Hsing-I Huang 1,2,3,4,*, Jhao-Yin Lin 1,3 and Sheng-Hung Chen 1,3
1
Research Center for Emerging Viral Infections, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 33303, Taiwan
2
Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 33303, Taiwan
3
Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 33303, Taiwan
4
Department of Pediatrics, Chang Gung Memorial Hospital, Linkou 33303, Taiwan
*
Author to whom correspondence should be addressed.
Viruses 2019, 11(12), 1121; https://doi.org/10.3390/v11121121
Received: 30 September 2019 / Revised: 21 November 2019 / Accepted: 1 December 2019 / Published: 4 December 2019
(This article belongs to the Special Issue Human Picornaviruses)
Enterovirus 71 (EV71) can invade the central nervous system (CNS) and cause neurological disease. Accumulating evidence indicates that EV71 can directly infect neurons in the CNS. Innate immune responses in the CNS have been known to play an essential role in limiting pathogen infections. Thus, investigating the effects of EV71 infection of neural cells is important for understanding disease pathogenesis. In this study, human neural cells were infected with EV71, and interferonβ (IFNβ) expression was examined. Our results show that IFNβ expression was upregulated in EV71-infected neural cells via pattern recognition receptors (PRRs) sensing of virus RNA. The PRRs Toll-like receptor 3 (TLR3), Toll-like receptor 8 (TLR8), and melanoma differentiation-associated gene-5 (MDA-5), but not retinoic acid-inducible gene-I (RIG-I) and Toll-like receptor 7 (TLR7), were found to be EV71-mediated IFNβ induction. Although viral proteins exhibited the ability to cleave mitochondrial antiviral signaling protein (MAVS) and Toll/IL-1 receptor (TIR) domain-containing adaptor-inducing IFN-β (TRIF) in neural cells, levels of viral protein expression were low in these cells. Furthermore, neural cells efficiently produced IFNβ transcripts upon EV71 vRNA stimulation. Treating infected cells with anti-IFNβ antibodies resulted in increased virus replication, indicating that IFNβ release may play a role in limiting viral growth. These results indicate that EV71 infection can induce IFNβ expression in neural cells through PRR pathways. View Full-Text
Keywords: EV71; IFNβ; neural cells; pattern recognition receptor; interferon-stimulated genes EV71; IFNβ; neural cells; pattern recognition receptor; interferon-stimulated genes
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Huang, H.-I.; Lin, J.-Y.; Chen, S.-H. EV71 Infection Induces IFNβ Expression in Neural Cells. Viruses 2019, 11, 1121.

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