A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles

ABSTRACT Enterovirus A71 (EV-A71) is the major pathogen of hand, foot, and mouth disease (HFMD); in some severe cases, it could develop into central nervous system (CNS) disease such as aseptic meningitis, encephalitis, and neurogenic pulmonary edema in children under 5 years. The EV-A71 pathogenesi...

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Autores principales:	Jiaqi Gu, Jing Wu, Yuwen Cao, Xinran Zou, Xiaonan Jia, Yiqian Yin, Li Shen, Daihua Fang, Lingxiang Mao
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2020
Materias:	enterovirus A71 (EV-A71) mouse model small extracellular vesicles (sEVs) central nervous system (CNS) pathogenesis Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/35d0123509284c29998d3c6783df7f07
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spelling	oai:doaj.org-article:35d0123509284c29998d3c6783df7f072021-11-15T15:30:51ZA Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles10.1128/mSphere.00377-202379-5042https://doaj.org/article/35d0123509284c29998d3c6783df7f072020-08-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mSphere.00377-20https://doaj.org/toc/2379-5042ABSTRACT Enterovirus A71 (EV-A71) is the major pathogen of hand, foot, and mouth disease (HFMD); in some severe cases, it could develop into central nervous system (CNS) disease such as aseptic meningitis, encephalitis, and neurogenic pulmonary edema in children under 5 years. The EV-A71 pathogenesis which is involved with the CNS is unclear due to the lack of a simple and reliable mouse model thus far. Most clinical EV-A71 isolates could not effectively infect the neonatal mouse, which used to be an EV-A71 infection model. The small extracellular vesicles (sEVs) released from clinical EV-A71 isolate-infected cells were infectious in cell lines and could cause a high viral replication in mice. Neonatal ICR mice were injected intraperitoneally with these infectious sEVs and showed more weight loss and higher mortality than those mice injected with the clinical EV-A71 isolate. By using these sEVs, we provided a simple and effective method by which we can generate a stable and valuable animal model for the studies of EV-A71 pathogenesis and therapy. IMPORTANCE EV-A71 was supposed to infect the CNS through the neural pathway and the circulation of the blood in previous studies. Reverse axon transport had been confirmed as an important pathway for EV-A71 to infect the CNS; however, it is still unknown how EV-A71 infects the CNS through the circulation of the blood. Combined with the infectivity of sEVs secreted from EV-A71-infected cells and the characteristic that sEVs could cross the blood-brain barrier, we considered that sEVs may play a vital role in EV-A71 pathogenesis of the CNS.Jiaqi GuJing WuYuwen CaoXinran ZouXiaonan JiaYiqian YinLi ShenDaihua FangLingxiang MaoAmerican Society for Microbiologyarticleenterovirus A71 (EV-A71)mouse modelsmall extracellular vesicles (sEVs)central nervous system (CNS)pathogenesisMicrobiologyQR1-502ENmSphere, Vol 5, Iss 4 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	enterovirus A71 (EV-A71) mouse model small extracellular vesicles (sEVs) central nervous system (CNS) pathogenesis Microbiology QR1-502
spellingShingle	enterovirus A71 (EV-A71) mouse model small extracellular vesicles (sEVs) central nervous system (CNS) pathogenesis Microbiology QR1-502 Jiaqi Gu Jing Wu Yuwen Cao Xinran Zou Xiaonan Jia Yiqian Yin Li Shen Daihua Fang Lingxiang Mao A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles
description	ABSTRACT Enterovirus A71 (EV-A71) is the major pathogen of hand, foot, and mouth disease (HFMD); in some severe cases, it could develop into central nervous system (CNS) disease such as aseptic meningitis, encephalitis, and neurogenic pulmonary edema in children under 5 years. The EV-A71 pathogenesis which is involved with the CNS is unclear due to the lack of a simple and reliable mouse model thus far. Most clinical EV-A71 isolates could not effectively infect the neonatal mouse, which used to be an EV-A71 infection model. The small extracellular vesicles (sEVs) released from clinical EV-A71 isolate-infected cells were infectious in cell lines and could cause a high viral replication in mice. Neonatal ICR mice were injected intraperitoneally with these infectious sEVs and showed more weight loss and higher mortality than those mice injected with the clinical EV-A71 isolate. By using these sEVs, we provided a simple and effective method by which we can generate a stable and valuable animal model for the studies of EV-A71 pathogenesis and therapy. IMPORTANCE EV-A71 was supposed to infect the CNS through the neural pathway and the circulation of the blood in previous studies. Reverse axon transport had been confirmed as an important pathway for EV-A71 to infect the CNS; however, it is still unknown how EV-A71 infects the CNS through the circulation of the blood. Combined with the infectivity of sEVs secreted from EV-A71-infected cells and the characteristic that sEVs could cross the blood-brain barrier, we considered that sEVs may play a vital role in EV-A71 pathogenesis of the CNS.
format	article
author	Jiaqi Gu Jing Wu Yuwen Cao Xinran Zou Xiaonan Jia Yiqian Yin Li Shen Daihua Fang Lingxiang Mao
author_facet	Jiaqi Gu Jing Wu Yuwen Cao Xinran Zou Xiaonan Jia Yiqian Yin Li Shen Daihua Fang Lingxiang Mao
author_sort	Jiaqi Gu
title	A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles
title_short	A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles
title_full	A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles
title_fullStr	A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles
title_full_unstemmed	A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles
title_sort	mouse model for infection with enterovirus a71 in small extracellular vesicles
publisher	American Society for Microbiology
publishDate	2020
url	https://doaj.org/article/35d0123509284c29998d3c6783df7f07
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A Mouse Model for Infection with Enterovirus A71 in Small Extracellular Vesicles

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