Porcine teschovirus 2 induces an incomplete autophagic response in PK-15 cells.
Identifieur interne : 000667 ( Main/Corpus ); précédent : 000666; suivant : 000668Porcine teschovirus 2 induces an incomplete autophagic response in PK-15 cells.
Auteurs : Yuanxing Gu ; Yingshan Zhou ; Xinfeng Shi ; Yongping Xin ; Ying Shan ; Cong Chen ; Tong Cao ; Weihuan Fang ; Xiaoliang LiSource :
- Archives of virology [ 1432-8798 ] ; 2018.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Androstadienes (pharmacology), Animals (MeSH), Autophagy (drug effects), Autophagy (genetics), Autophagy-Related Protein 5 (antagonists & inhibitors), Autophagy-Related Protein 5 (genetics), Autophagy-Related Protein 5 (metabolism), Cell Line (MeSH), Epithelial Cells (drug effects), Epithelial Cells (metabolism), Epithelial Cells (virology), Gene Expression Regulation (MeSH), Genes, Reporter (MeSH), Green Fluorescent Proteins (genetics), Green Fluorescent Proteins (metabolism), Host-Pathogen Interactions (MeSH), Kidney (MeSH), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), RNA, Small Interfering (genetics), RNA, Small Interfering (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), Swine (MeSH), Teschovirus (drug effects), Teschovirus (genetics), Teschovirus (growth & development), Teschovirus (metabolism), Virus Replication (drug effects), Virus Replication (genetics), Wortmannin (MeSH).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , antagonists & inhibitors : Autophagy-Related Protein 5.
- chemical , genetics : Autophagy-Related Protein 5, Green Fluorescent Proteins, Microtubule-Associated Proteins, RNA, Small Interfering.
- chemical , metabolism : Autophagy-Related Protein 5, Green Fluorescent Proteins, Microtubule-Associated Proteins, RNA, Small Interfering.
- chemical , pharmacology : Adenine, Androstadienes, Sirolimus.
- drug effects : Autophagy, Epithelial Cells, Teschovirus, Virus Replication.
- genetics : Autophagy, Teschovirus, Virus Replication.
- growth & development : Teschovirus.
- metabolism : Epithelial Cells, Teschovirus.
- virology : Epithelial Cells.
- Animals, Cell Line, Gene Expression Regulation, Genes, Reporter, Host-Pathogen Interactions, Kidney, Signal Transduction, Swine, Wortmannin.
Abstract
Autophagy is a homeostatic process that has been shown to be vital in the innate immune defense against pathogens. However, little is known about the regulatory role of autophagy in porcine teschovirus 2 (PTV-2) replication. In this study, we found that PTV-2 infection induces a strong increase in GFP-LC3 punctae and endogenous LC3 lipidation. However, PTV-2 infection did not enhance autophagic protein degradation. When cellular autophagy was pharmacologically inhibited by wortmannin or 3-methyladenine, PTV-2 replication increased. The increase in virus yield via autophagy inhibition was further confirmed by silencing atg5, which is required for autophagy. Furthermore, PTV-2 replication was suppressed when autophagy was activated by rapamycin. Together, the results suggest that PTV-2 infection activates incomplete autophagy and that autophagy then inhibits further PTV-2 replication.
DOI: 10.1007/s00705-017-3652-2
PubMed: 29177545
Links to Exploration step
pubmed:29177545Le document en format XML
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<term>Autophagy-Related Protein 5 (antagonists & inhibitors)</term>
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<term>Epithelial Cells (virology)</term>
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<term>Microtubule-Associated Proteins (metabolism)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>RNA, Small Interfering (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
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<term>Teschovirus (growth & development)</term>
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<front><div type="abstract" xml:lang="en">Autophagy is a homeostatic process that has been shown to be vital in the innate immune defense against pathogens. However, little is known about the regulatory role of autophagy in porcine teschovirus 2 (PTV-2) replication. In this study, we found that PTV-2 infection induces a strong increase in GFP-LC3 punctae and endogenous LC3 lipidation. However, PTV-2 infection did not enhance autophagic protein degradation. When cellular autophagy was pharmacologically inhibited by wortmannin or 3-methyladenine, PTV-2 replication increased. The increase in virus yield via autophagy inhibition was further confirmed by silencing atg5, which is required for autophagy. Furthermore, PTV-2 replication was suppressed when autophagy was activated by rapamycin. Together, the results suggest that PTV-2 infection activates incomplete autophagy and that autophagy then inhibits further PTV-2 replication.</div>
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<Abstract><AbstractText>Autophagy is a homeostatic process that has been shown to be vital in the innate immune defense against pathogens. However, little is known about the regulatory role of autophagy in porcine teschovirus 2 (PTV-2) replication. In this study, we found that PTV-2 infection induces a strong increase in GFP-LC3 punctae and endogenous LC3 lipidation. However, PTV-2 infection did not enhance autophagic protein degradation. When cellular autophagy was pharmacologically inhibited by wortmannin or 3-methyladenine, PTV-2 replication increased. The increase in virus yield via autophagy inhibition was further confirmed by silencing atg5, which is required for autophagy. Furthermore, PTV-2 replication was suppressed when autophagy was activated by rapamycin. Together, the results suggest that PTV-2 infection activates incomplete autophagy and that autophagy then inhibits further PTV-2 replication.</AbstractText>
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