Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication

In this study, we investigated the correlation between the mechanism involved in porcine epidemic diarrhea virus (PEDV) replication and autophagic flux. In this study, we found that as PEDV replicated, production of LC3-II was significantly induced up to 24 h post-infection (hpi). Interestingly, alt...

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Autores principales: Park, Jae-Yeon, Ryu, Jihoon, Hong, Eui-Ju, Shin, Hyun-Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9142955/
https://www.ncbi.nlm.nih.gov/pubmed/35632790
http://dx.doi.org/10.3390/v14051050
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author Park, Jae-Yeon
Ryu, Jihoon
Hong, Eui-Ju
Shin, Hyun-Jin
author_facet Park, Jae-Yeon
Ryu, Jihoon
Hong, Eui-Ju
Shin, Hyun-Jin
author_sort Park, Jae-Yeon
collection PubMed
description In this study, we investigated the correlation between the mechanism involved in porcine epidemic diarrhea virus (PEDV) replication and autophagic flux. In this study, we found that as PEDV replicated, production of LC3-II was significantly induced up to 24 h post-infection (hpi). Interestingly, although there was significant production of LC3-II, greater p62 accumulation was simultaneously found. Pretreatment with rapamycin significantly induced PEDV replication, but autolysosome formation was reduced. These results were confirmed by the evaluation of ATG5/ATG12 and LAMP1/LAMP2. Taken together, we conclude that PEDV infection induces autophagosome formation but inhibits autolysosome formation during replication.
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spelling pubmed-91429552022-05-29 Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication Park, Jae-Yeon Ryu, Jihoon Hong, Eui-Ju Shin, Hyun-Jin Viruses Article In this study, we investigated the correlation between the mechanism involved in porcine epidemic diarrhea virus (PEDV) replication and autophagic flux. In this study, we found that as PEDV replicated, production of LC3-II was significantly induced up to 24 h post-infection (hpi). Interestingly, although there was significant production of LC3-II, greater p62 accumulation was simultaneously found. Pretreatment with rapamycin significantly induced PEDV replication, but autolysosome formation was reduced. These results were confirmed by the evaluation of ATG5/ATG12 and LAMP1/LAMP2. Taken together, we conclude that PEDV infection induces autophagosome formation but inhibits autolysosome formation during replication. MDPI 2022-05-15 /pmc/articles/PMC9142955/ /pubmed/35632790 http://dx.doi.org/10.3390/v14051050 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Park, Jae-Yeon
Ryu, Jihoon
Hong, Eui-Ju
Shin, Hyun-Jin
Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication
title Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication
title_full Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication
title_fullStr Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication
title_full_unstemmed Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication
title_short Porcine Epidemic Diarrhea Virus Infection Induces Autophagosome Formation but Inhibits Autolysosome Formation during Replication
title_sort porcine epidemic diarrhea virus infection induces autophagosome formation but inhibits autolysosome formation during replication
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9142955/
https://www.ncbi.nlm.nih.gov/pubmed/35632790
http://dx.doi.org/10.3390/v14051050
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