c-Jun N-terminal kinase activity is required for efficient respiratory syncytial virus production.
Identifieur interne : 000A53 ( Main/Exploration ); précédent : 000A52; suivant : 000A54c-Jun N-terminal kinase activity is required for efficient respiratory syncytial virus production.
Auteurs : Leon Caly [Australie] ; Hong-Mei Li [Australie] ; Marie A. Bogoyevitch [Australie] ; David A. Jans [Australie]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2017.
Descripteurs français
- KwdFr :
- Activation enzymatique, Assemblage viral (physiologie), Cellules A549, Humains, Inhibiteurs de protéines kinases (pharmacologie), Interactions hôte-pathogène (), Interactions hôte-pathogène (génétique), Interactions hôte-pathogène (physiologie), Libération de particules virales (physiologie), Mitogen-Activated Protein Kinase 8 (antagonistes et inhibiteurs), Mitogen-Activated Protein Kinase 8 (génétique), Mitogen-Activated Protein Kinase 8 (métabolisme), Mitogen-Activated Protein Kinase 9 (antagonistes et inhibiteurs), Mitogen-Activated Protein Kinase 9 (génétique), Mitogen-Activated Protein Kinase 9 (métabolisme), Petit ARN interférent (génétique), Réplication virale (physiologie), Techniques de knock-down de gènes, Virion (physiologie), Virus respiratoire syncytial humain (), Virus respiratoire syncytial humain (pathogénicité), Virus respiratoire syncytial humain (physiologie).
- MESH :
- antagonistes et inhibiteurs : Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9.
- génétique : Interactions hôte-pathogène, Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9, Petit ARN interférent.
- métabolisme : Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9.
- pathogénicité : Virus respiratoire syncytial humain.
- pharmacologie : Inhibiteurs de protéines kinases.
- physiologie : Assemblage viral, Interactions hôte-pathogène, Libération de particules virales, Réplication virale, Virion, Virus respiratoire syncytial humain.
- Activation enzymatique, Cellules A549, Humains, Interactions hôte-pathogène, Techniques de knock-down de gènes, Virus respiratoire syncytial humain.
English descriptors
- KwdEn :
- A549 Cells, Enzyme Activation, Gene Knockdown Techniques, Host-Pathogen Interactions (drug effects), Host-Pathogen Interactions (genetics), Host-Pathogen Interactions (physiology), Humans, Mitogen-Activated Protein Kinase 8 (antagonists & inhibitors), Mitogen-Activated Protein Kinase 8 (genetics), Mitogen-Activated Protein Kinase 8 (metabolism), Mitogen-Activated Protein Kinase 9 (antagonists & inhibitors), Mitogen-Activated Protein Kinase 9 (genetics), Mitogen-Activated Protein Kinase 9 (metabolism), Protein Kinase Inhibitors (pharmacology), RNA, Small Interfering (genetics), Respiratory Syncytial Virus, Human (drug effects), Respiratory Syncytial Virus, Human (pathogenicity), Respiratory Syncytial Virus, Human (physiology), Virion (physiology), Virus Assembly (physiology), Virus Release (physiology), Virus Replication (physiology).
- MESH :
- chemical , antagonists & inhibitors : Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9.
- drug effects : Host-Pathogen Interactions, Respiratory Syncytial Virus, Human.
- genetics : Host-Pathogen Interactions, Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9, RNA, Small Interfering.
- chemical , metabolism : Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9.
- pathogenicity : Respiratory Syncytial Virus, Human.
- chemical , pharmacology : Protein Kinase Inhibitors.
- physiology : Host-Pathogen Interactions, Respiratory Syncytial Virus, Human, Virion, Virus Assembly, Virus Release, Virus Replication.
- A549 Cells, Enzyme Activation, Gene Knockdown Techniques, Humans.
Abstract
Respiratory syncytial virus (RSV) is a major cause of respiratory infections in infants and the elderly, leading to more deaths than influenza each year worldwide. With no RSV antiviral or efficacious vaccine currently available, improved understanding of the host-RSV interaction is urgently required. Here we examine the contribution to RSV infection of the host stress-regulated c-Jun N-terminal kinase (JNK), for the first time. Peak JNK1/2 phosphoactivation is observed at ∼24 h post-infection, correlating with the time of virus assembly. The release of infectious RSV virions from infected cells was significantly reduced by either JNK1/2 siRNA knockdown or treatment with the JNK-specific inhibitor, JNK-IN-VIII. High resolution microscopy confirmed RSV accumulation in the host cell cytoplasm. The results implicate JNK1/2 as a key host factor for RSV virus production, raising the possibility of agents targeting JNK activity as potential anti-RSV therapeutics.
DOI: 10.1016/j.bbrc.2017.01.005
PubMed: 28062184
Affiliations:
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Le document en format XML
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Bogoyevitch</name><affiliation wicri:level="4"><nlm:affiliation>Cell Signalling Research Laboratories, Bio21 Institute, Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria, 3010, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Cell Signalling Research Laboratories, Bio21 Institute, Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria, 3010</wicri:regionArea><orgName type="university">Université de Melbourne</orgName><placeName><settlement type="city">Melbourne</settlement><region type="état">Victoria (État)</region></placeName></affiliation></author><author><name sortKey="Jans, David A" sort="Jans, David A" uniqKey="Jans D" first="David A" last="Jans">David A. Jans</name><affiliation wicri:level="1"><nlm:affiliation>Nuclear Signalling Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia. 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Protein Kinase 8 (genetics)</term><term>Mitogen-Activated Protein Kinase 8 (metabolism)</term><term>Mitogen-Activated Protein Kinase 9 (antagonists & inhibitors)</term><term>Mitogen-Activated Protein Kinase 9 (genetics)</term><term>Mitogen-Activated Protein Kinase 9 (metabolism)</term><term>Protein Kinase Inhibitors (pharmacology)</term><term>RNA, Small Interfering (genetics)</term><term>Respiratory Syncytial Virus, Human (drug effects)</term><term>Respiratory Syncytial Virus, Human (pathogenicity)</term><term>Respiratory Syncytial Virus, Human (physiology)</term><term>Virion (physiology)</term><term>Virus Assembly (physiology)</term><term>Virus Release (physiology)</term><term>Virus Replication (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique</term><term>Assemblage viral (physiologie)</term><term>Cellules A549</term><term>Humains</term><term>Inhibiteurs de protéines kinases (pharmacologie)</term><term>Interactions hôte-pathogène ()</term><term>Interactions hôte-pathogène (génétique)</term><term>Interactions hôte-pathogène (physiologie)</term><term>Libération de particules virales (physiologie)</term><term>Mitogen-Activated Protein Kinase 8 (antagonistes et inhibiteurs)</term><term>Mitogen-Activated Protein Kinase 8 (génétique)</term><term>Mitogen-Activated Protein Kinase 8 (métabolisme)</term><term>Mitogen-Activated Protein Kinase 9 (antagonistes et inhibiteurs)</term><term>Mitogen-Activated Protein Kinase 9 (génétique)</term><term>Mitogen-Activated Protein Kinase 9 (métabolisme)</term><term>Petit ARN interférent (génétique)</term><term>Réplication virale (physiologie)</term><term>Techniques de knock-down de gènes</term><term>Virion (physiologie)</term><term>Virus respiratoire syncytial humain ()</term><term>Virus respiratoire syncytial humain (pathogénicité)</term><term>Virus respiratoire syncytial humain (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & 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qualifier="metabolism" xml:lang="en"><term>Mitogen-Activated Protein Kinase 8</term><term>Mitogen-Activated Protein Kinase 9</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Mitogen-Activated Protein Kinase 8</term><term>Mitogen-Activated Protein Kinase 9</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Respiratory Syncytial Virus, Human</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus respiratoire syncytial humain</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Inhibiteurs de protéines kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Protein Kinase Inhibitors</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Assemblage viral</term><term>Interactions hôte-pathogène</term><term>Libération de particules virales</term><term>Réplication virale</term><term>Virion</term><term>Virus respiratoire syncytial humain</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Host-Pathogen Interactions</term><term>Respiratory Syncytial Virus, Human</term><term>Virion</term><term>Virus Assembly</term><term>Virus Release</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Enzyme Activation</term><term>Gene Knockdown Techniques</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term><term>Cellules A549</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Techniques de knock-down de gènes</term><term>Virus respiratoire syncytial humain</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Respiratory syncytial virus (RSV) is a major cause of respiratory infections in infants and the elderly, leading to more deaths than influenza each year worldwide. With no RSV antiviral or efficacious vaccine currently available, improved understanding of the host-RSV interaction is urgently required. Here we examine the contribution to RSV infection of the host stress-regulated c-Jun N-terminal kinase (JNK), for the first time. Peak JNK1/2 phosphoactivation is observed at ∼24 h post-infection, correlating with the time of virus assembly. The release of infectious RSV virions from infected cells was significantly reduced by either JNK1/2 siRNA knockdown or treatment with the JNK-specific inhibitor, JNK-IN-VIII. High resolution microscopy confirmed RSV accumulation in the host cell cytoplasm. The results implicate JNK1/2 as a key host factor for RSV virus production, raising the possibility of agents targeting JNK activity as potential anti-RSV therapeutics.</div></front></TEI><affiliations><list><country><li>Australie</li></country><region><li>Victoria (État)</li></region><settlement><li>Melbourne</li></settlement><orgName><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><noRegion><name sortKey="Caly, Leon" sort="Caly, Leon" uniqKey="Caly L" first="Leon" last="Caly">Leon Caly</name></noRegion><name sortKey="Bogoyevitch, Marie A" sort="Bogoyevitch, Marie A" uniqKey="Bogoyevitch M" first="Marie A" last="Bogoyevitch">Marie A. Bogoyevitch</name><name sortKey="Jans, David A" sort="Jans, David A" uniqKey="Jans D" first="David A" last="Jans">David A. Jans</name><name sortKey="Li, Hong Mei" sort="Li, Hong Mei" uniqKey="Li H" first="Hong-Mei" last="Li">Hong-Mei Li</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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