Replication of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E is inhibited by the drug FK506.
Identifieur interne : 001C74 ( Main/Exploration ); précédent : 001C73; suivant : 001C75Replication of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E is inhibited by the drug FK506.
Auteurs : Javier Carbajo-Lozoya [Allemagne] ; Marcel A. Müller ; Stephan Kallies ; Volker Thiel ; Christian Drosten ; Albrecht Von BrunnSource :
- Virus research [ 1872-7492 ] ; 2012.
Descripteurs français
- KwdFr :
- Cellules Caco-2, Coronavirus humain 229E (), Coronavirus humain 229E (physiologie), Coronavirus humain NL63 (), Coronavirus humain NL63 (physiologie), Humains, Infections à coronavirus (génétique), Infections à coronavirus (métabolisme), Infections à coronavirus (virologie), Protéines de liaison au tacrolimus (génétique), Protéines de liaison au tacrolimus (métabolisme), Réplication virale (), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Tacrolimus (pharmacologie), Virus du SRAS (), Virus du SRAS (physiologie).
- MESH :
- génétique : Infections à coronavirus, Protéines de liaison au tacrolimus, Syndrome respiratoire aigu sévère.
- métabolisme : Infections à coronavirus, Protéines de liaison au tacrolimus, Syndrome respiratoire aigu sévère.
- pharmacologie : Tacrolimus.
- physiologie : Coronavirus humain 229E, Coronavirus humain NL63, Virus du SRAS.
- virologie : Infections à coronavirus, Syndrome respiratoire aigu sévère.
- Cellules Caco-2, Coronavirus humain 229E, Coronavirus humain NL63, Humains, Réplication virale, Virus du SRAS.
English descriptors
- KwdEn :
- Caco-2 Cells, Coronavirus 229E, Human (drug effects), Coronavirus 229E, Human (physiology), Coronavirus Infections (genetics), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Coronavirus NL63, Human (drug effects), Coronavirus NL63, Human (physiology), Humans, SARS Virus (drug effects), SARS Virus (physiology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Tacrolimus (pharmacology), Tacrolimus Binding Proteins (genetics), Tacrolimus Binding Proteins (metabolism), Virus Replication (drug effects).
- MESH :
- chemical , genetics : Tacrolimus Binding Proteins.
- chemical , metabolism : Tacrolimus Binding Proteins.
- chemical , pharmacology : Tacrolimus.
- drug effects : Coronavirus 229E, Human, Coronavirus NL63, Human, SARS Virus, Virus Replication.
- genetics : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- metabolism : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- physiology : Coronavirus 229E, Human, Coronavirus NL63, Human, SARS Virus.
- virology : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- Caco-2 Cells, Humans.
Abstract
Recent research has shown that Coronavirus (CoV) replication depends on active immunophilin pathways. Here we demonstrate that the drug FK506 (Tacrolimus) inhibited strongly the growth of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E at low, non-cytotoxic concentrations in cell culture. As shown by plaque titration, qPCR, Luciferase- and green fluorescent protein (GFP) reporter gene expression, replication was diminished by several orders of magnitude. Knockdown of the cellular FK506-binding proteins FKBP1A and FKBP1B in CaCo2 cells prevented replication of HCoV-NL63, suggesting the requirement of these members of the immunophilin family for virus growth.
DOI: 10.1016/j.virusres.2012.02.002
PubMed: 22349148
Affiliations:
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Le document en format XML
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virale</term><term>Virus du SRAS</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent research has shown that Coronavirus (CoV) replication depends on active immunophilin pathways. Here we demonstrate that the drug FK506 (Tacrolimus) inhibited strongly the growth of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E at low, non-cytotoxic concentrations in cell culture. As shown by plaque titration, qPCR, Luciferase- and green fluorescent protein (GFP) reporter gene expression, replication was diminished by several orders of magnitude. Knockdown of the cellular FK506-binding proteins FKBP1A and FKBP1B in CaCo2 cells prevented replication of HCoV-NL63, suggesting the requirement of these members of the immunophilin family for virus growth.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Bavière</li><li>District de Haute-Bavière</li></region><settlement><li>Munich</li></settlement><orgName><li>Université Louis-et-Maximilien de Munich</li></orgName></list><tree><noCountry><name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name><name sortKey="Kallies, Stephan" sort="Kallies, Stephan" uniqKey="Kallies S" first="Stephan" last="Kallies">Stephan Kallies</name><name sortKey="Muller, Marcel A" sort="Muller, Marcel A" uniqKey="Muller M" first="Marcel A" last="Müller">Marcel A. Müller</name><name sortKey="Thiel, Volker" sort="Thiel, Volker" uniqKey="Thiel V" first="Volker" last="Thiel">Volker Thiel</name><name sortKey="Von Brunn, Albrecht" sort="Von Brunn, Albrecht" uniqKey="Von Brunn A" first="Albrecht" last="Von Brunn">Albrecht Von Brunn</name></noCountry><country name="Allemagne"><region name="Bavière"><name sortKey="Carbajo Lozoya, Javier" sort="Carbajo Lozoya, Javier" uniqKey="Carbajo Lozoya J" first="Javier" last="Carbajo-Lozoya">Javier Carbajo-Lozoya</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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