Combined action of type I and type III interferon restricts initial replication of severe acute respiratory syndrome coronavirus in the lung but fails to inhibit systemic virus spread.
Identifieur interne : 001D48 ( Main/Exploration ); précédent : 001D47; suivant : 001D49Combined action of type I and type III interferon restricts initial replication of severe acute respiratory syndrome coronavirus in the lung but fails to inhibit systemic virus spread.
Auteurs : Tanel Mahlak Iv [Allemagne] ; Daniel Ritz [Allemagne] ; Markus Mordstein [Allemagne] ; Marta L. Dediego [Espagne] ; Luis Enjuanes [Espagne] ; Marcel A. Müller [Allemagne] ; Christian Drosten [Allemagne] ; Peter Staeheli [Allemagne]Source :
- The Journal of general virology [ 1465-2099 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux, Facteur de transcription STAT-1 (déficit), Facteur de transcription STAT-1 (génétique), Facteur de transcription STAT-1 (immunologie), Interféron de type I (immunologie), Interférons (immunologie), Poumon (immunologie), Poumon (virologie), Récepteur interféron (déficit), Récepteur interféron (génétique), Récepteur interféron (immunologie), Récepteur à l'interféron alpha-bêta (déficit), Récepteur à l'interféron alpha-bêta (génétique), Récepteur à l'interféron alpha-bêta (immunologie), Réplication virale (immunologie), Souris, Souris de lignée C57BL, Souris knockout, Virus du SRAS (immunologie), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- déficit : Facteur de transcription STAT-1, Récepteur interféron, Récepteur à l'interféron alpha-bêta.
- génétique : Facteur de transcription STAT-1, Récepteur interféron, Récepteur à l'interféron alpha-bêta.
- immunologie : Facteur de transcription STAT-1, Interféron de type I, Interférons, Poumon, Récepteur interféron, Récepteur à l'interféron alpha-bêta, Réplication virale, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- physiologie : Virus du SRAS.
- virologie : Poumon.
- Animaux, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Animals, Interferon Type I (immunology), Interferons (immunology), Lung (immunology), Lung (virology), Mice, Mice, Inbred C57BL, Mice, Knockout, Receptor, Interferon alpha-beta (deficiency), Receptor, Interferon alpha-beta (genetics), Receptor, Interferon alpha-beta (immunology), Receptors, Interferon (deficiency), Receptors, Interferon (genetics), Receptors, Interferon (immunology), SARS Virus (immunology), SARS Virus (pathogenicity), SARS Virus (physiology), STAT1 Transcription Factor (deficiency), STAT1 Transcription Factor (genetics), STAT1 Transcription Factor (immunology), Virus Replication (immunology).
- MESH :
- chemical , deficiency : Receptor, Interferon alpha-beta, Receptors, Interferon, STAT1 Transcription Factor.
- chemical , genetics : Receptor, Interferon alpha-beta, Receptors, Interferon, STAT1 Transcription Factor.
- chemical , immunology : Interferon Type I, Interferons, Receptor, Interferon alpha-beta, Receptors, Interferon, STAT1 Transcription Factor.
- immunology : Lung, SARS Virus, Virus Replication.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- virology : Lung.
- Animals, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
STAT1-deficient mice are more susceptible to infection with severe acute respiratory syndrome coronavirus (SARS-CoV) than type I interferon (IFN) receptor-deficient mice. We used mice lacking functional receptors for both type I and type III IFN (double knockout, dKO) to evaluate the possibility that type III IFN plays a decisive role in SARS-CoV protection. We found that viral peak titres in lungs of dKO and STAT1-deficient mice were similar, but significantly higher than in wild-type mice. The kinetics of viral clearance from the lung were also comparable in dKO and STAT1-deficient mice. Surprisingly, however, infected dKO mice remained healthy, whereas infected STAT1-deficient mice developed liver pathology and eventually succumbed to neurological disease. Our data suggest that the failure of STAT1-deficient mice to control initial SARS-CoV replication efficiently in the lung is due to impaired type I and type III IFN signalling, whereas the failure to control subsequent systemic viral spread is due to unrelated defects in STAT1-deficient mice.
DOI: 10.1099/vir.0.046284-0
PubMed: 22956738
Affiliations:
- Allemagne, Espagne
- Bade-Wurtemberg, Communauté de Madrid, District de Cologne, District de Fribourg-en-Brisgau, Rhénanie-du-Nord-Westphalie
- Bonn, Fribourg-en-Brisgau, Madrid
- Université autonome de Madrid
Links toward previous steps (curation, corpus...)
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Le document en format XML
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but fails to inhibit systemic virus spread.</title><author><name sortKey="Mahlak Iv, Tanel" sort="Mahlak Iv, Tanel" uniqKey="Mahlak Iv T" first="Tanel" last="Mahlak Iv">Tanel Mahlak Iv</name><affiliation wicri:level="3"><nlm:affiliation>Spemann Graduate School of Biology and Medicine (SGBM), University of Freiburg, 79104 Freiburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Spemann Graduate School of Biology and Medicine (SGBM), University of Freiburg, 79104 Freiburg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Fribourg-en-Brisgau</region><settlement type="city">Fribourg-en-Brisgau</settlement></placeName></affiliation></author><author><name sortKey="Ritz, Daniel" sort="Ritz, Daniel" uniqKey="Ritz D" first="Daniel" last="Ritz">Daniel Ritz</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Virology, University of Bonn Medical Center, 53127 Bonn, 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Dediego</name><affiliation wicri:level="4"><nlm:affiliation>Centro Nacional de Biotecnología (CNB-CSIC), Department of Molecular and Cell Biology, Campus Universidad Autónoma de Madrid, 28049 Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Centro Nacional de Biotecnología (CNB-CSIC), Department of Molecular and Cell Biology, Campus Universidad Autónoma de Madrid, 28049 Madrid</wicri:regionArea><placeName><region nuts="2" type="communauté">Communauté de Madrid</region><settlement type="city">Madrid</settlement></placeName><orgName type="university">Université autonome de Madrid</orgName></affiliation></author><author><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name><affiliation wicri:level="4"><nlm:affiliation>Centro Nacional de Biotecnología (CNB-CSIC), Department of Molecular and Cell Biology, Campus Universidad Autónoma de Madrid, 28049 Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Centro Nacional de Biotecnología (CNB-CSIC), Department of Molecular and Cell Biology, Campus Universidad Autónoma de Madrid, 28049 Madrid</wicri:regionArea><placeName><region nuts="2" type="communauté">Communauté de Madrid</region><settlement type="city">Madrid</settlement></placeName><orgName type="university">Université autonome de Madrid</orgName></affiliation></author><author><name sortKey="Muller, Marcel A" sort="Muller, Marcel A" uniqKey="Muller M" first="Marcel A" last="Müller">Marcel A. Müller</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Virology, University of Bonn Medical Center, 53127 Bonn, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Virology, University of Bonn Medical Center, 53127 Bonn</wicri:regionArea><placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region><region type="district" nuts="2">District de Cologne</region><settlement type="city">Bonn</settlement></placeName></affiliation></author><author><name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Virology, University of Bonn Medical Center, 53127 Bonn, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Virology, University of Bonn Medical Center, 53127 Bonn</wicri:regionArea><placeName><region type="land" 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type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Interferon Type I (immunology)</term><term>Interferons (immunology)</term><term>Lung (immunology)</term><term>Lung (virology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Receptor, Interferon alpha-beta (deficiency)</term><term>Receptor, Interferon alpha-beta (genetics)</term><term>Receptor, Interferon alpha-beta (immunology)</term><term>Receptors, Interferon (deficiency)</term><term>Receptors, Interferon (genetics)</term><term>Receptors, Interferon (immunology)</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>SARS Virus (physiology)</term><term>STAT1 Transcription Factor (deficiency)</term><term>STAT1 Transcription Factor (genetics)</term><term>STAT1 Transcription Factor (immunology)</term><term>Virus Replication (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Facteur de transcription STAT-1 (déficit)</term><term>Facteur de transcription STAT-1 (génétique)</term><term>Facteur de transcription STAT-1 (immunologie)</term><term>Interféron de type I (immunologie)</term><term>Interférons (immunologie)</term><term>Poumon (immunologie)</term><term>Poumon (virologie)</term><term>Récepteur interféron (déficit)</term><term>Récepteur interféron (génétique)</term><term>Récepteur interféron (immunologie)</term><term>Récepteur à l'interféron alpha-bêta (déficit)</term><term>Récepteur à l'interféron alpha-bêta (génétique)</term><term>Récepteur à l'interféron alpha-bêta (immunologie)</term><term>Réplication virale (immunologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptor, Interferon alpha-beta</term><term>Receptors, Interferon</term><term>STAT1 Transcription Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptor, Interferon alpha-beta</term><term>Receptors, Interferon</term><term>STAT1 Transcription Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon Type I</term><term>Interferons</term><term>Receptor, Interferon alpha-beta</term><term>Receptors, Interferon</term><term>STAT1 Transcription Factor</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteur de transcription STAT-1</term><term>Récepteur interféron</term><term>Récepteur à l'interféron alpha-bêta</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de transcription STAT-1</term><term>Récepteur interféron</term><term>Récepteur à l'interféron alpha-bêta</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteur de transcription STAT-1</term><term>Interféron de type I</term><term>Interférons</term><term>Poumon</term><term>Récepteur interféron</term><term>Récepteur à l'interféron alpha-bêta</term><term>Réplication virale</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term><term>SARS Virus</term><term>Virus Replication</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="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">STAT1-deficient mice are more susceptible to infection with severe acute respiratory syndrome coronavirus (SARS-CoV) than type I interferon (IFN) receptor-deficient mice. We used mice lacking functional receptors for both type I and type III IFN (double knockout, dKO) to evaluate the possibility that type III IFN plays a decisive role in SARS-CoV protection. We found that viral peak titres in lungs of dKO and STAT1-deficient mice were similar, but significantly higher than in wild-type mice. The kinetics of viral clearance from the lung were also comparable in dKO and STAT1-deficient mice. Surprisingly, however, infected dKO mice remained healthy, whereas infected STAT1-deficient mice developed liver pathology and eventually succumbed to neurological disease. Our data suggest that the failure of STAT1-deficient mice to control initial SARS-CoV replication efficiently in the lung is due to impaired type I and type III IFN signalling, whereas the failure to control subsequent systemic viral spread is due to unrelated defects in STAT1-deficient mice.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Espagne</li></country><region><li>Bade-Wurtemberg</li><li>Communauté de Madrid</li><li>District de Cologne</li><li>District de Fribourg-en-Brisgau</li><li>Rhénanie-du-Nord-Westphalie</li></region><settlement><li>Bonn</li><li>Fribourg-en-Brisgau</li><li>Madrid</li></settlement><orgName><li>Université autonome de Madrid</li></orgName></list><tree><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Mahlak Iv, Tanel" sort="Mahlak Iv, Tanel" uniqKey="Mahlak Iv T" first="Tanel" last="Mahlak Iv">Tanel Mahlak Iv</name></region><name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name><name sortKey="Mordstein, Markus" sort="Mordstein, Markus" uniqKey="Mordstein M" first="Markus" last="Mordstein">Markus Mordstein</name><name sortKey="Muller, Marcel A" sort="Muller, Marcel A" uniqKey="Muller M" first="Marcel A" last="Müller">Marcel A. Müller</name><name sortKey="Ritz, Daniel" sort="Ritz, Daniel" uniqKey="Ritz D" first="Daniel" last="Ritz">Daniel Ritz</name><name sortKey="Staeheli, Peter" sort="Staeheli, Peter" uniqKey="Staeheli P" first="Peter" last="Staeheli">Peter Staeheli</name></country><country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Dediego, Marta L" sort="Dediego, Marta L" uniqKey="Dediego M" first="Marta L" last="Dediego">Marta L. Dediego</name></region><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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