Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis

Human parechovirus type 3 (PeV-A3) infection has been recognized as an emerging etiologic factor causing severe nerve disease or sepsis in infants and young children. But the neuropathogenic mechanisms of PeV-A3 remain unknown. To understand the pathogenesis of PeV-A3 infection in the neuronal syste...

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Autores principales: Ming-Wei Jan, Hong-Lin Su, Tsung-Hsien Chang, Kuen-Jer Tsai
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Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/2b8c417aad7f48fb99cf8a71a04fcdc7
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spelling oai:doaj.org-article:2b8c417aad7f48fb99cf8a71a04fcdc72021-11-30T21:33:07ZCharacterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis1664-322410.3389/fimmu.2021.753683https://doaj.org/article/2b8c417aad7f48fb99cf8a71a04fcdc72021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.753683/fullhttps://doaj.org/toc/1664-3224Human parechovirus type 3 (PeV-A3) infection has been recognized as an emerging etiologic factor causing severe nerve disease or sepsis in infants and young children. But the neuropathogenic mechanisms of PeV-A3 remain unknown. To understand the pathogenesis of PeV-A3 infection in the neuronal system, PeV-A3-mediated cytopathic effects were analyzed in human glioblastoma cells and neuroblastoma cells. PeV-A3 induced interferons and inflammatory cytokine expression in these neuronal cells. The pronounced cytopathic effects accompanied with activation of death signaling pathways of apoptosis, autophagy, and pyroptosis were detected. A new experimental disease model of parechovirus encephalitis was established. In the disease model, intracranial inoculation with PeV-A3 in C57BL/6 neonatal mice showed body weight loss, hindlimb paralysis, and approximately 20% mortality. PeV-A3 infection in the hippocampus and cortex regions of the neonatal mouse brain was revealed. Mechanistic assay supported the in vitro results, indicating detection of PeV-A3 replication, inflammatory cytokine expression, and death signaling transduction in mouse brain tissues. These in vitro and in vivo studies revealed that the activation of death signaling and inflammation responses is involved in PeV-A3-mediated neurological disorders. The present results might account for some of the PeV-A3-associated clinical manifestations.Ming-Wei JanMing-Wei JanHong-Lin SuTsung-Hsien ChangKuen-Jer TsaiKuen-Jer TsaiFrontiers Media S.A.articleparechovirus A3cytopathic effectinflammationneuronal diseasesinfectious modelImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic parechovirus A3
cytopathic effect
inflammation
neuronal diseases
infectious model
Immunologic diseases. Allergy
RC581-607
spellingShingle parechovirus A3
cytopathic effect
inflammation
neuronal diseases
infectious model
Immunologic diseases. Allergy
RC581-607
Ming-Wei Jan
Ming-Wei Jan
Hong-Lin Su
Tsung-Hsien Chang
Kuen-Jer Tsai
Kuen-Jer Tsai
Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis
description Human parechovirus type 3 (PeV-A3) infection has been recognized as an emerging etiologic factor causing severe nerve disease or sepsis in infants and young children. But the neuropathogenic mechanisms of PeV-A3 remain unknown. To understand the pathogenesis of PeV-A3 infection in the neuronal system, PeV-A3-mediated cytopathic effects were analyzed in human glioblastoma cells and neuroblastoma cells. PeV-A3 induced interferons and inflammatory cytokine expression in these neuronal cells. The pronounced cytopathic effects accompanied with activation of death signaling pathways of apoptosis, autophagy, and pyroptosis were detected. A new experimental disease model of parechovirus encephalitis was established. In the disease model, intracranial inoculation with PeV-A3 in C57BL/6 neonatal mice showed body weight loss, hindlimb paralysis, and approximately 20% mortality. PeV-A3 infection in the hippocampus and cortex regions of the neonatal mouse brain was revealed. Mechanistic assay supported the in vitro results, indicating detection of PeV-A3 replication, inflammatory cytokine expression, and death signaling transduction in mouse brain tissues. These in vitro and in vivo studies revealed that the activation of death signaling and inflammation responses is involved in PeV-A3-mediated neurological disorders. The present results might account for some of the PeV-A3-associated clinical manifestations.
format article
author Ming-Wei Jan
Ming-Wei Jan
Hong-Lin Su
Tsung-Hsien Chang
Kuen-Jer Tsai
Kuen-Jer Tsai
author_facet Ming-Wei Jan
Ming-Wei Jan
Hong-Lin Su
Tsung-Hsien Chang
Kuen-Jer Tsai
Kuen-Jer Tsai
author_sort Ming-Wei Jan
title Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis
title_short Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis
title_full Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis
title_fullStr Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis
title_full_unstemmed Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis
title_sort characterization of pathogenesis and inflammatory responses to experimental parechovirus encephalitis
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/2b8c417aad7f48fb99cf8a71a04fcdc7
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AT tsunghsienchang characterizationofpathogenesisandinflammatoryresponsestoexperimentalparechovirusencephalitis
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