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Cell Host Microbe. 2016 Nov 9;20(5):631-641. doi: 10.1016/j.chom.2016.09.013. Epub 2016 Oct 27.

ICAM-5/Telencephalin Is a Functional Entry Receptor for Enterovirus D68.

Author information

1
First Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province 130021, China. Electronic address: wwei6@jlu.edu.cn.
2
First Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province 130021, China.
3
Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang 310058, China.
4
Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD 21205, USA; Cellphire, Inc., 9430 Key West Avenue, Rockville, MD 20850, USA.
5
First Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province 130021, China; Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang 310058, China; Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD 21205, USA. Electronic address: xyu2@jhu.edu.

Abstract

Enterovirus D68 (EV-D68) is a member of the Picornaviridae family. Although EV-D68-associated infection was once considered rare, it has been increasing in recent years. EV-D68 infection is most frequently associated with respiratory illness. However, it has also been implicated in a polio-like neurological disorder, acute flaccid myelitis. Although sialic acid has been implicated in EV-D68 entry, the existence of a protein receptor has yet to be clarified. Here we identify neuron-specific intercellular adhesion molecule 5 (ICAM-5/telencephalin) as a cellular receptor for sialic acid-dependent and -independent EV-D68 viruses. EV-D68 bound specifically and efficiently to ICAM-5, and replication of EV-D68 in diverse cell types was inhibited by soluble ICAM-5 fragments. ICAM-5 silencing attenuated EV-D68 replication in permissive cells, and ICAM-5 expression in non-permissive cells allowed EV-D68 replication. The discovery of a neuron-specific adhesion molecule as an EV-D68 receptor has important implications for EV-D68 pathogenesis and may facilitate the development of novel intervention strategies.

KEYWORDS:

EV-D68; ICAM-5/telencephalin; acute flaccid myelitis; enterovirus; entry receptor; picornaviridae; respiratory illness

PMID:
27923705
DOI:
10.1016/j.chom.2016.09.013
[Indexed for MEDLINE]
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