BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells

The levels of cellular reactive oxygen species (ROS) and ATP as well as the mitochondrial membrane potential (MMP) in response to bovine herpesvirus 1 (BHV-1) infection of MDBK cells were measured, respectively. BHV-1 infection increased ROS production which depended on viral entry, and de novo prot...

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Autores principales: Zhu, Liqian, Yuan, Chen, Zhang, Dong, Ma, Yan, Ding, Xiuyan, Zhu, Guoqiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Short Report
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802597/
https://www.ncbi.nlm.nih.gov/pubmed/27000063
http://dx.doi.org/10.1186/s13567-016-0332-2
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author Zhu, Liqian
Yuan, Chen
Zhang, Dong
Ma, Yan
Ding, Xiuyan
Zhu, Guoqiang
author_facet Zhu, Liqian
Yuan, Chen
Zhang, Dong
Ma, Yan
Ding, Xiuyan
Zhu, Guoqiang
author_sort Zhu, Liqian
collection PubMed
description The levels of cellular reactive oxygen species (ROS) and ATP as well as the mitochondrial membrane potential (MMP) in response to bovine herpesvirus 1 (BHV-1) infection of MDBK cells were measured, respectively. BHV-1 infection increased ROS production which depended on viral entry, and de novo protein expression and/or DNA replication. Vice versa, excessive ROS was required for efficient viral replication. Levels of both ATP and MMP were significantly decreased after BHV-1 infection. Interestingly, the loss of MMP was ameliorated by ROS depression. Collectively, ROS dependent mitochondrial damage and ultimately disruption of energy metabolism (ATP depletion) are a potential pathogenic mechanism for BHV-1 infection.
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spelling pubmed-48025972016-03-22 BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells Zhu, Liqian Yuan, Chen Zhang, Dong Ma, Yan Ding, Xiuyan Zhu, Guoqiang Vet Res Short Report The levels of cellular reactive oxygen species (ROS) and ATP as well as the mitochondrial membrane potential (MMP) in response to bovine herpesvirus 1 (BHV-1) infection of MDBK cells were measured, respectively. BHV-1 infection increased ROS production which depended on viral entry, and de novo protein expression and/or DNA replication. Vice versa, excessive ROS was required for efficient viral replication. Levels of both ATP and MMP were significantly decreased after BHV-1 infection. Interestingly, the loss of MMP was ameliorated by ROS depression. Collectively, ROS dependent mitochondrial damage and ultimately disruption of energy metabolism (ATP depletion) are a potential pathogenic mechanism for BHV-1 infection. BioMed Central 2016-03-22 2016 /pmc/articles/PMC4802597/ /pubmed/27000063 http://dx.doi.org/10.1186/s13567-016-0332-2 Text en © Zhu et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Short Report
Zhu, Liqian
Yuan, Chen
Zhang, Dong
Ma, Yan
Ding, Xiuyan
Zhu, Guoqiang
BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
title BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
title_full BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
title_fullStr BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
title_full_unstemmed BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
title_short BHV-1 induced oxidative stress contributes to mitochondrial dysfunction in MDBK cells
title_sort bhv-1 induced oxidative stress contributes to mitochondrial dysfunction in mdbk cells
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802597/
https://www.ncbi.nlm.nih.gov/pubmed/27000063
http://dx.doi.org/10.1186/s13567-016-0332-2
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