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Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication
Enterovirus A71 (EV-A71) is a major pathogen that causes severe and fatal cases of hand-foot-and-mouth disease (HFMD), which is an infectious disease that endangers children’s health. However, the pathogenic mechanisms underlying these severe clinical and pathological features remain incompletely un...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9554258/ https://www.ncbi.nlm.nih.gov/pubmed/36246276 http://dx.doi.org/10.3389/fmicb.2022.961942 |
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author | Yang, Xiuwen Chen, Jiayi Lu, Zixin Huang, Shan Zhang, Shihao Cai, Jintai Zhou, Yezhen Cao, Guanhua Yu, Jianhai Qin, Zhiran Zhao, Wei Zhang, Bao Zhu, Li |
author_facet | Yang, Xiuwen Chen, Jiayi Lu, Zixin Huang, Shan Zhang, Shihao Cai, Jintai Zhou, Yezhen Cao, Guanhua Yu, Jianhai Qin, Zhiran Zhao, Wei Zhang, Bao Zhu, Li |
author_sort | Yang, Xiuwen |
collection | PubMed |
description | Enterovirus A71 (EV-A71) is a major pathogen that causes severe and fatal cases of hand-foot-and-mouth disease (HFMD), which is an infectious disease that endangers children’s health. However, the pathogenic mechanisms underlying these severe clinical and pathological features remain incompletely understood. Metabolism and stress are known to play critical roles in multiple stages of the replication of viruses. Lipid metabolism and ER stress is an important characterization post viral infection. EV-A71 infection alters the perturbations of intracellular lipid homeostasis and induces ER stress. The characterizations induced by viral infections are essential for optimal virus replication and may be potential antiviral targets. In this study, we found that the addition of the chemical drug of ER stress, PKR IN, an inhibitor, or Tunicamycin, an activator, could significantly reduce viral replication with the decrease of lipid. The replication of viruses was reduced by Chemical reagent TOFA, an inhibitor of acetyl-CoA carboxylase (ACC) or C75, an inhibitor of fatty acid synthase (FASN), while enhanced by oleic acid (OA), which is a kind of exogenous supplement of triacylglycerol. The pharmacochemical reagent of carnitine palmitoyltransferase 1 (CPT1) called Etomoxir could knock down CPT1 to induce EV-A71 replication to decrease. This suggests that lipid, rather than ER stress, is the main factor affecting EV-A71 replication. In conclusion, this study revealed that it is the β-oxidation of lipid that plays a core role, not ER stress, which is only a concomitant change without restrictive effect, on virus replication. |
format | Online Article Text |
id | pubmed-9554258 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-95542582022-10-13 Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication Yang, Xiuwen Chen, Jiayi Lu, Zixin Huang, Shan Zhang, Shihao Cai, Jintai Zhou, Yezhen Cao, Guanhua Yu, Jianhai Qin, Zhiran Zhao, Wei Zhang, Bao Zhu, Li Front Microbiol Microbiology Enterovirus A71 (EV-A71) is a major pathogen that causes severe and fatal cases of hand-foot-and-mouth disease (HFMD), which is an infectious disease that endangers children’s health. However, the pathogenic mechanisms underlying these severe clinical and pathological features remain incompletely understood. Metabolism and stress are known to play critical roles in multiple stages of the replication of viruses. Lipid metabolism and ER stress is an important characterization post viral infection. EV-A71 infection alters the perturbations of intracellular lipid homeostasis and induces ER stress. The characterizations induced by viral infections are essential for optimal virus replication and may be potential antiviral targets. In this study, we found that the addition of the chemical drug of ER stress, PKR IN, an inhibitor, or Tunicamycin, an activator, could significantly reduce viral replication with the decrease of lipid. The replication of viruses was reduced by Chemical reagent TOFA, an inhibitor of acetyl-CoA carboxylase (ACC) or C75, an inhibitor of fatty acid synthase (FASN), while enhanced by oleic acid (OA), which is a kind of exogenous supplement of triacylglycerol. The pharmacochemical reagent of carnitine palmitoyltransferase 1 (CPT1) called Etomoxir could knock down CPT1 to induce EV-A71 replication to decrease. This suggests that lipid, rather than ER stress, is the main factor affecting EV-A71 replication. In conclusion, this study revealed that it is the β-oxidation of lipid that plays a core role, not ER stress, which is only a concomitant change without restrictive effect, on virus replication. Frontiers Media S.A. 2022-09-28 /pmc/articles/PMC9554258/ /pubmed/36246276 http://dx.doi.org/10.3389/fmicb.2022.961942 Text en Copyright © 2022 Yang, Chen, Lu, Huang, Zhang, Cai, Zhou, Cao, Yu, Qin, Zhao, Zhang and Zhu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Yang, Xiuwen Chen, Jiayi Lu, Zixin Huang, Shan Zhang, Shihao Cai, Jintai Zhou, Yezhen Cao, Guanhua Yu, Jianhai Qin, Zhiran Zhao, Wei Zhang, Bao Zhu, Li Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication |
title | Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication |
title_full | Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication |
title_fullStr | Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication |
title_full_unstemmed | Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication |
title_short | Enterovirus A71 utilizes host cell lipid β-oxidation to promote its replication |
title_sort | enterovirus a71 utilizes host cell lipid β-oxidation to promote its replication |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9554258/ https://www.ncbi.nlm.nih.gov/pubmed/36246276 http://dx.doi.org/10.3389/fmicb.2022.961942 |
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