Cargando…

Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways

Porcine hemagglutinating encephalomyelitis is an acute, highly contagious disease in piglets that is caused by the porcine hemagglutinating encephalomyelitis virus (PHEV). However, the pathogenesis of PHEV and the relationship between PHEV and the host cells are not fully understood. In this study,...

Descripción completa

Detalles Bibliográficos
Autores principales: Lan, Yungang, Zhao, Kui, Wang, Gaili, Dong, Bo, Zhao, Jiakuan, Tang, Bo, Lu, Huijun, Gao, Wei, Chang, Lingzhu, Jin, Zhao, Gao, Feng, He, Wenqi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114423/
https://www.ncbi.nlm.nih.gov/pubmed/23770152
http://dx.doi.org/10.1016/j.virusres.2013.05.019
_version_ 1783513882512326656
author Lan, Yungang
Zhao, Kui
Wang, Gaili
Dong, Bo
Zhao, Jiakuan
Tang, Bo
Lu, Huijun
Gao, Wei
Chang, Lingzhu
Jin, Zhao
Gao, Feng
He, Wenqi
author_facet Lan, Yungang
Zhao, Kui
Wang, Gaili
Dong, Bo
Zhao, Jiakuan
Tang, Bo
Lu, Huijun
Gao, Wei
Chang, Lingzhu
Jin, Zhao
Gao, Feng
He, Wenqi
author_sort Lan, Yungang
collection PubMed
description Porcine hemagglutinating encephalomyelitis is an acute, highly contagious disease in piglets that is caused by the porcine hemagglutinating encephalomyelitis virus (PHEV). However, the pathogenesis of PHEV and the relationship between PHEV and the host cells are not fully understood. In this study, we investigated whether the PHEV-induced cytopathic effect (CPE) was caused by apoptosis. Replication of PHEV in a porcine kidney-derived cell line (PK-15 cells) caused an extensive CPE, leading to the destruction of the entire monolayer and the death of the infected cells. Staining with Hoechst 33,342 revealed morphological changes in the nuclei and chromatin fragmentation. In addition, PHEV caused DNA fragmentation detectable by agarose gel electrophoresis 48 h post-infection, increasing with the incubation time. The percentage of apoptotic cells increased with the incubation time and reached a maximum at 96 h post-infection, as determined using flow cytometry and fluorescence microscopy of cells that were stained with annexin V-FITC and propidium iodide (PI). Moreover, as is commonly observed for coronavirus infections of other animals, the activities of the effecter caspase, caspase-3, and the initiator caspases, caspase-8 and caspase-9, which are representative factors in the death receptor-mediated apoptotic pathway and the mitochondrial apoptotic pathway, respectively, were increased in PHEV-infected PK-15 cells. Moreover, the tripeptide pan-ICE (caspase) inhibitor Z-VAD-FMK blocked PHEV-induced apoptosis but did not have an effect on virus production by 96 h post-infection. These results suggested that PHEV induces apoptosis in PK-15 cells via a caspase-dependent pathway. Apoptotic death of infected cells is detrimental to animals because it causes cell and tissue destruction. Although the pathological characteristics of PHEV are largely unknown, apoptosis may be the pathological basis of the lesions resulting from PHEV infection.
format Online
Article
Text
id pubmed-7114423
institution National Center for Biotechnology Information
language English
publishDate 2013
publisher Elsevier B.V.
record_format MEDLINE/PubMed
spelling pubmed-71144232020-04-02 Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways Lan, Yungang Zhao, Kui Wang, Gaili Dong, Bo Zhao, Jiakuan Tang, Bo Lu, Huijun Gao, Wei Chang, Lingzhu Jin, Zhao Gao, Feng He, Wenqi Virus Res Short Communication Porcine hemagglutinating encephalomyelitis is an acute, highly contagious disease in piglets that is caused by the porcine hemagglutinating encephalomyelitis virus (PHEV). However, the pathogenesis of PHEV and the relationship between PHEV and the host cells are not fully understood. In this study, we investigated whether the PHEV-induced cytopathic effect (CPE) was caused by apoptosis. Replication of PHEV in a porcine kidney-derived cell line (PK-15 cells) caused an extensive CPE, leading to the destruction of the entire monolayer and the death of the infected cells. Staining with Hoechst 33,342 revealed morphological changes in the nuclei and chromatin fragmentation. In addition, PHEV caused DNA fragmentation detectable by agarose gel electrophoresis 48 h post-infection, increasing with the incubation time. The percentage of apoptotic cells increased with the incubation time and reached a maximum at 96 h post-infection, as determined using flow cytometry and fluorescence microscopy of cells that were stained with annexin V-FITC and propidium iodide (PI). Moreover, as is commonly observed for coronavirus infections of other animals, the activities of the effecter caspase, caspase-3, and the initiator caspases, caspase-8 and caspase-9, which are representative factors in the death receptor-mediated apoptotic pathway and the mitochondrial apoptotic pathway, respectively, were increased in PHEV-infected PK-15 cells. Moreover, the tripeptide pan-ICE (caspase) inhibitor Z-VAD-FMK blocked PHEV-induced apoptosis but did not have an effect on virus production by 96 h post-infection. These results suggested that PHEV induces apoptosis in PK-15 cells via a caspase-dependent pathway. Apoptotic death of infected cells is detrimental to animals because it causes cell and tissue destruction. Although the pathological characteristics of PHEV are largely unknown, apoptosis may be the pathological basis of the lesions resulting from PHEV infection. Elsevier B.V. 2013-09 2013-06-12 /pmc/articles/PMC7114423/ /pubmed/23770152 http://dx.doi.org/10.1016/j.virusres.2013.05.019 Text en Copyright © 2013 Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Short Communication
Lan, Yungang
Zhao, Kui
Wang, Gaili
Dong, Bo
Zhao, Jiakuan
Tang, Bo
Lu, Huijun
Gao, Wei
Chang, Lingzhu
Jin, Zhao
Gao, Feng
He, Wenqi
Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
title Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
title_full Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
title_fullStr Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
title_full_unstemmed Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
title_short Porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
title_sort porcine hemagglutinating encephalomyelitis virus induces apoptosis in a porcine kidney cell line via caspase-dependent pathways
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114423/
https://www.ncbi.nlm.nih.gov/pubmed/23770152
http://dx.doi.org/10.1016/j.virusres.2013.05.019
work_keys_str_mv AT lanyungang porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT zhaokui porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT wanggaili porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT dongbo porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT zhaojiakuan porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT tangbo porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT luhuijun porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT gaowei porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT changlingzhu porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT jinzhao porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT gaofeng porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways
AT hewenqi porcinehemagglutinatingencephalomyelitisvirusinducesapoptosisinaporcinekidneycelllineviacaspasedependentpathways