The SARS-coronavirus-host interactome: identification of cyclophilins as target for pan-coronavirus inhibitors.
Identifieur interne : 001418 ( PubMed/Checkpoint ); précédent : 001417; suivant : 001419The SARS-coronavirus-host interactome: identification of cyclophilins as target for pan-coronavirus inhibitors.
Auteurs : Susanne Pfefferle [Allemagne] ; Julia Schöpf ; Manfred Kögl ; Caroline C. Friedel ; Marcel A. Müller ; Javier Carbajo-Lozoya ; Thorsten Stellberger ; Ekatarina Von Dall'Armi ; Petra Herzog ; Stefan Kallies ; Daniela Niemeyer ; Vanessa Ditt ; Thomas Kuri ; Roland Züst ; Ksenia Pumpor ; Rolf Hilgenfeld ; Frank Schwarz ; Ralf Zimmer ; Imke Steffen ; Friedemann Weber ; Volker Thiel ; Georg Herrler ; Heinz-Jürgen Thiel ; Christel Schwegmann-Wessels ; Stefan Pöhlmann ; Jürgen Haas ; Christian Drosten ; Albrecht Von BrunnSource :
- PLoS pathogens [ 1553-7374 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux, Antiviraux (usage thérapeutique), Cartographie d'interactions entre protéines, Cellules Caco-2, Cellules HEK293, Cellules Jurkat, Cellules Vero, Ciclosporine (pharmacologie), Cyclophilines (), Cyclophilines (antagonistes et inhibiteurs), Cyclophilines (métabolisme), Humains, Inhibiteurs de protéases (pharmacologie), Interactions hôte-pathogène, Protéines virales (métabolisme), Réplication virale (), Syndrome respiratoire aigu sévère (traitement médicamenteux), Techniques de double hybride, Virus du SRAS (), Virus du SRAS (pathogénicité).
- MESH :
- antagonistes et inhibiteurs : Cyclophilines.
- métabolisme : Cyclophilines, Protéines virales.
- pathogénicité : Virus du SRAS.
- pharmacologie : Ciclosporine, Inhibiteurs de protéases.
- traitement médicamenteux : Syndrome respiratoire aigu sévère.
- usage thérapeutique : Antiviraux.
- Animaux, Cartographie d'interactions entre protéines, Cellules Caco-2, Cellules HEK293, Cellules Jurkat, Cellules Vero, Cyclophilines, Humains, Interactions hôte-pathogène, Réplication virale, Techniques de double hybride, Virus du SRAS.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (therapeutic use), Caco-2 Cells, Chlorocebus aethiops, Cyclophilins (antagonists & inhibitors), Cyclophilins (drug effects), Cyclophilins (metabolism), Cyclosporine (pharmacology), HEK293 Cells, Host-Pathogen Interactions, Humans, Jurkat Cells, Protease Inhibitors (pharmacology), Protein Interaction Mapping, SARS Virus (drug effects), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (drug therapy), Two-Hybrid System Techniques, Vero Cells, Viral Proteins (metabolism), Virus Replication (drug effects).
- MESH :
- chemical , antagonists & inhibitors : Cyclophilins.
- chemical , drug effects : Cyclophilins.
- chemical , metabolism : Cyclophilins, Viral Proteins.
- chemical , pharmacology : Cyclosporine, Protease Inhibitors.
- chemical , therapeutic use : Antiviral Agents.
- drug effects : SARS Virus, Virus Replication.
- drug therapy : Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- Animals, Caco-2 Cells, Chlorocebus aethiops, HEK293 Cells, Host-Pathogen Interactions, Humans, Jurkat Cells, Protein Interaction Mapping, Two-Hybrid System Techniques, Vero Cells.
Abstract
Coronaviruses (CoVs) are important human and animal pathogens that induce fatal respiratory, gastrointestinal and neurological disease. The outbreak of the severe acute respiratory syndrome (SARS) in 2002/2003 has demonstrated human vulnerability to (Coronavirus) CoV epidemics. Neither vaccines nor therapeutics are available against human and animal CoVs. Knowledge of host cell proteins that take part in pivotal virus-host interactions could define broad-spectrum antiviral targets. In this study, we used a systems biology approach employing a genome-wide yeast-two hybrid interaction screen to identify immunopilins (PPIA, PPIB, PPIH, PPIG, FKBP1A, FKBP1B) as interaction partners of the CoV non-structural protein 1 (Nsp1). These molecules modulate the Calcineurin/NFAT pathway that plays an important role in immune cell activation. Overexpression of NSP1 and infection with live SARS-CoV strongly increased signalling through the Calcineurin/NFAT pathway and enhanced the induction of interleukin 2, compatible with late-stage immunopathogenicity and long-term cytokine dysregulation as observed in severe SARS cases. Conversely, inhibition of cyclophilins by cyclosporine A (CspA) blocked the replication of CoVs of all genera, including SARS-CoV, human CoV-229E and -NL-63, feline CoV, as well as avian infectious bronchitis virus. Non-immunosuppressive derivatives of CspA might serve as broad-range CoV inhibitors applicable against emerging CoVs as well as ubiquitous pathogens of humans and livestock.
DOI: 10.1371/journal.ppat.1002331
PubMed: 22046132
Affiliations:
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Friedel</name></author><author><name sortKey="Muller, Marcel A" sort="Muller, Marcel A" uniqKey="Muller M" first="Marcel A" last="Müller">Marcel A. Müller</name></author><author><name sortKey="Carbajo Lozoya, Javier" sort="Carbajo Lozoya, Javier" uniqKey="Carbajo Lozoya J" first="Javier" last="Carbajo-Lozoya">Javier Carbajo-Lozoya</name></author><author><name sortKey="Stellberger, Thorsten" sort="Stellberger, Thorsten" uniqKey="Stellberger T" first="Thorsten" last="Stellberger">Thorsten Stellberger</name></author><author><name sortKey="Von Dall Armi, Ekatarina" sort="Von Dall Armi, Ekatarina" uniqKey="Von Dall Armi E" first="Ekatarina" last="Von Dall'Armi">Ekatarina Von Dall'Armi</name></author><author><name sortKey="Herzog, Petra" sort="Herzog, Petra" uniqKey="Herzog P" first="Petra" last="Herzog">Petra Herzog</name></author><author><name sortKey="Kallies, Stefan" sort="Kallies, Stefan" uniqKey="Kallies S" first="Stefan" last="Kallies">Stefan Kallies</name></author><author><name sortKey="Niemeyer, Daniela" sort="Niemeyer, Daniela" uniqKey="Niemeyer D" first="Daniela" last="Niemeyer">Daniela Niemeyer</name></author><author><name 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uniqKey="Steffen I" first="Imke" last="Steffen">Imke Steffen</name></author><author><name sortKey="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name></author><author><name sortKey="Thiel, Volker" sort="Thiel, Volker" uniqKey="Thiel V" first="Volker" last="Thiel">Volker Thiel</name></author><author><name sortKey="Herrler, Georg" sort="Herrler, Georg" uniqKey="Herrler G" first="Georg" last="Herrler">Georg Herrler</name></author><author><name sortKey="Thiel, Heinz Jurgen" sort="Thiel, Heinz Jurgen" uniqKey="Thiel H" first="Heinz-Jürgen" last="Thiel">Heinz-Jürgen Thiel</name></author><author><name sortKey="Schwegmann Wessels, Christel" sort="Schwegmann Wessels, Christel" uniqKey="Schwegmann Wessels C" first="Christel" last="Schwegmann-Wessels">Christel Schwegmann-Wessels</name></author><author><name sortKey="Pohlmann, Stefan" sort="Pohlmann, Stefan" uniqKey="Pohlmann S" first="Stefan" last="Pöhlmann">Stefan Pöhlmann</name></author><author><name sortKey="Haas, Jurgen" sort="Haas, Jurgen" uniqKey="Haas J" first="Jürgen" last="Haas">Jürgen Haas</name></author><author><name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name></author><author><name sortKey="Von Brunn, Albrecht" sort="Von Brunn, Albrecht" uniqKey="Von Brunn A" first="Albrecht" last="Von Brunn">Albrecht Von Brunn</name></author></analytic><series><title level="j">PLoS pathogens</title><idno type="eISSN">1553-7374</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiviral Agents (therapeutic use)</term><term>Caco-2 Cells</term><term>Chlorocebus aethiops</term><term>Cyclophilins (antagonists & inhibitors)</term><term>Cyclophilins (drug effects)</term><term>Cyclophilins (metabolism)</term><term>Cyclosporine (pharmacology)</term><term>HEK293 Cells</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Jurkat Cells</term><term>Protease Inhibitors (pharmacology)</term><term>Protein Interaction Mapping</term><term>SARS Virus (drug effects)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (drug therapy)</term><term>Two-Hybrid System Techniques</term><term>Vero Cells</term><term>Viral Proteins (metabolism)</term><term>Virus Replication (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antiviraux (usage thérapeutique)</term><term>Cartographie d'interactions entre protéines</term><term>Cellules Caco-2</term><term>Cellules HEK293</term><term>Cellules Jurkat</term><term>Cellules Vero</term><term>Ciclosporine (pharmacologie)</term><term>Cyclophilines ()</term><term>Cyclophilines (antagonistes et inhibiteurs)</term><term>Cyclophilines (métabolisme)</term><term>Humains</term><term>Inhibiteurs de protéases (pharmacologie)</term><term>Interactions hôte-pathogène</term><term>Protéines virales (métabolisme)</term><term>Réplication virale ()</term><term>Syndrome respiratoire aigu sévère (traitement médicamenteux)</term><term>Techniques de double hybride</term><term>Virus du SRAS ()</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cyclophilins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Cyclophilins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclophilins</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cyclosporine</term><term>Protease Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiviral Agents</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Cyclophilines</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>SARS Virus</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cyclophilines</term><term>Protéines virales</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Ciclosporine</term><term>Inhibiteurs de protéases</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antiviraux</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Caco-2 Cells</term><term>Chlorocebus aethiops</term><term>HEK293 Cells</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Jurkat Cells</term><term>Protein Interaction Mapping</term><term>Two-Hybrid System Techniques</term><term>Vero Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cartographie d'interactions entre protéines</term><term>Cellules Caco-2</term><term>Cellules HEK293</term><term>Cellules Jurkat</term><term>Cellules Vero</term><term>Cyclophilines</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Réplication virale</term><term>Techniques de double hybride</term><term>Virus du SRAS</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Coronaviruses (CoVs) are important human and animal pathogens that induce fatal respiratory, gastrointestinal and neurological disease. The outbreak of the severe acute respiratory syndrome (SARS) in 2002/2003 has demonstrated human vulnerability to (Coronavirus) CoV epidemics. Neither vaccines nor therapeutics are available against human and animal CoVs. Knowledge of host cell proteins that take part in pivotal virus-host interactions could define broad-spectrum antiviral targets. In this study, we used a systems biology approach employing a genome-wide yeast-two hybrid interaction screen to identify immunopilins (PPIA, PPIB, PPIH, PPIG, FKBP1A, FKBP1B) as interaction partners of the CoV non-structural protein 1 (Nsp1). These molecules modulate the Calcineurin/NFAT pathway that plays an important role in immune cell activation. Overexpression of NSP1 and infection with live SARS-CoV strongly increased signalling through the Calcineurin/NFAT pathway and enhanced the induction of interleukin 2, compatible with late-stage immunopathogenicity and long-term cytokine dysregulation as observed in severe SARS cases. Conversely, inhibition of cyclophilins by cyclosporine A (CspA) blocked the replication of CoVs of all genera, including SARS-CoV, human CoV-229E and -NL-63, feline CoV, as well as avian infectious bronchitis virus. Non-immunosuppressive derivatives of CspA might serve as broad-range CoV inhibitors applicable against emerging CoVs as well as ubiquitous pathogens of humans and livestock.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22046132</PMID><DateCompleted><Year>2012</Year><Month>02</Month><Day>23</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1553-7374</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>10</Issue><PubDate><Year>2011</Year><Month>Oct</Month></PubDate></JournalIssue><Title>PLoS pathogens</Title><ISOAbbreviation>PLoS Pathog.</ISOAbbreviation></Journal><ArticleTitle>The SARS-coronavirus-host interactome: identification of cyclophilins as target for pan-coronavirus inhibitors.</ArticleTitle><Pagination><MedlinePgn>e1002331</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.ppat.1002331</ELocationID><Abstract><AbstractText>Coronaviruses (CoVs) are important human and animal pathogens that induce fatal respiratory, gastrointestinal and neurological disease. The outbreak of the severe acute respiratory syndrome (SARS) in 2002/2003 has demonstrated human vulnerability to (Coronavirus) CoV epidemics. Neither vaccines nor therapeutics are available against human and animal CoVs. Knowledge of host cell proteins that take part in pivotal virus-host interactions could define broad-spectrum antiviral targets. In this study, we used a systems biology approach employing a genome-wide yeast-two hybrid interaction screen to identify immunopilins (PPIA, PPIB, PPIH, PPIG, FKBP1A, FKBP1B) as interaction partners of the CoV non-structural protein 1 (Nsp1). These molecules modulate the Calcineurin/NFAT pathway that plays an important role in immune cell activation. Overexpression of NSP1 and infection with live SARS-CoV strongly increased signalling through the Calcineurin/NFAT pathway and enhanced the induction of interleukin 2, compatible with late-stage immunopathogenicity and long-term cytokine dysregulation as observed in severe SARS cases. Conversely, inhibition of cyclophilins by cyclosporine A (CspA) blocked the replication of CoVs of all genera, including SARS-CoV, human CoV-229E and -NL-63, feline CoV, as well as avian infectious bronchitis virus. Non-immunosuppressive derivatives of CspA might serve as broad-range CoV inhibitors applicable against emerging CoVs as well as ubiquitous pathogens of humans and livestock.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pfefferle</LastName><ForeName>Susanne</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Bernhard-Nocht-Institute, Hamburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schöpf</LastName><ForeName>Julia</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Kögl</LastName><ForeName>Manfred</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Friedel</LastName><ForeName>Caroline C</ForeName><Initials>CC</Initials></Author><Author ValidYN="Y"><LastName>Müller</LastName><ForeName>Marcel A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Carbajo-Lozoya</LastName><ForeName>Javier</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Stellberger</LastName><ForeName>Thorsten</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>von Dall'Armi</LastName><ForeName>Ekatarina</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Herzog</LastName><ForeName>Petra</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Kallies</LastName><ForeName>Stefan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Niemeyer</LastName><ForeName>Daniela</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Ditt</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Kuri</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Züst</LastName><ForeName>Roland</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Pumpor</LastName><ForeName>Ksenia</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Hilgenfeld</LastName><ForeName>Rolf</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Schwarz</LastName><ForeName>Frank</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Zimmer</LastName><ForeName>Ralf</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Steffen</LastName><ForeName>Imke</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Weber</LastName><ForeName>Friedemann</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Thiel</LastName><ForeName>Volker</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Herrler</LastName><ForeName>Georg</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Thiel</LastName><ForeName>Heinz-Jürgen</ForeName><Initials>HJ</Initials></Author><Author ValidYN="Y"><LastName>Schwegmann-Wessels</LastName><ForeName>Christel</ForeName><Initials>C</Initials></Author><Author 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