CD8+ T Cells and Macrophages Regulate Pathogenesis in a Mouse Model of Middle East Respiratory Syndrome.
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Auteurs : Christopher M. Coleman [États-Unis] ; Jeanne M. Sisk [États-Unis] ; Gabor Halasz [États-Unis] ; Jixin Zhong [États-Unis] ; Sarah E. Beck [États-Unis] ; Krystal L. Matthews [États-Unis] ; Thiagarajan Venkataraman [États-Unis] ; Sanjay Rajagopalan [États-Unis] ; Christos A. Kyratsous [États-Unis] ; Matthew B. Frieman [États-Unis]Source :
- Journal of virology [ 1098-5514 ] ; 2017.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Animaux, Coronavirus du syndrome respiratoire du Moyen-Orient (génétique), Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité), Dipeptidyl peptidase 4 (génétique), Dipeptidyl peptidase 4 (immunologie), Déplétion lymphocytaire, Humains, Infections à coronavirus (anatomopathologie), Infections à coronavirus (génétique), Infections à coronavirus (immunologie), Infections à coronavirus (virologie), Interactions hôte-pathogène, Lymphocytes T CD4+ (immunologie), Lymphocytes T CD4+ (virologie), Lymphocytes T CD8+ (immunologie), Lymphocytes T CD8+ (virologie), Macrophages (immunologie), Macrophages (virologie), Modèles animaux de maladie humaine, Poumon (immunologie), Poumon (virologie), Pénétration virale, Récepteurs viraux (génétique), Récepteurs viraux (immunologie), Régions promotrices (génétique), Régulation de l'expression des gènes, Réplication virale, Souris, Souris de lignée C57BL, Souris transgéniques, Transcriptome, Transgènes.
- MESH :
- anatomopathologie : Infections à coronavirus.
- génétique : Coronavirus du syndrome respiratoire du Moyen-Orient, Dipeptidyl peptidase 4, Infections à coronavirus, Récepteurs viraux.
- immunologie : Coronavirus du syndrome respiratoire du Moyen-Orient, Dipeptidyl peptidase 4, Infections à coronavirus, Lymphocytes T CD4+, Lymphocytes T CD8+, Macrophages, Poumon, Récepteurs viraux.
- pathogénicité : Coronavirus du syndrome respiratoire du Moyen-Orient.
- virologie : Infections à coronavirus, Lymphocytes T CD4+, Lymphocytes T CD8+, Macrophages, Poumon.
- Analyse de profil d'expression de gènes, Animaux, Déplétion lymphocytaire, Humains, Interactions hôte-pathogène, Modèles animaux de maladie humaine, Pénétration virale, Régions promotrices (génétique), Régulation de l'expression des gènes, Réplication virale, Souris, Souris de lignée C57BL, Souris transgéniques, Transcriptome, Transgènes.
English descriptors
- KwdEn :
- Animals, CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (virology), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (virology), Coronavirus Infections (genetics), Coronavirus Infections (immunology), Coronavirus Infections (pathology), Coronavirus Infections (virology), Dipeptidyl Peptidase 4 (genetics), Dipeptidyl Peptidase 4 (immunology), Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Host-Pathogen Interactions, Humans, Lung (immunology), Lung (virology), Lymphocyte Depletion, Macrophages (immunology), Macrophages (virology), Mice, Mice, Inbred C57BL, Mice, Transgenic, Middle East Respiratory Syndrome Coronavirus (genetics), Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Promoter Regions, Genetic, Receptors, Virus (genetics), Receptors, Virus (immunology), Transcriptome, Transgenes, Virus Internalization, Virus Replication.
- MESH :
- chemical , genetics : Dipeptidyl Peptidase 4, Receptors, Virus.
- genetics : Coronavirus Infections, Middle East Respiratory Syndrome Coronavirus.
- immunology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Coronavirus Infections, Dipeptidyl Peptidase 4, Lung, Macrophages, Middle East Respiratory Syndrome Coronavirus, Receptors, Virus.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- pathology : Coronavirus Infections.
- virology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Coronavirus Infections, Lung, Macrophages.
- Animals, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Host-Pathogen Interactions, Humans, Lymphocyte Depletion, Mice, Mice, Inbred C57BL, Mice, Transgenic, Promoter Regions, Genetic, Transcriptome, Transgenes, Virus Internalization, Virus Replication.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) is an important emerging pathogen that was first described in 2012. While the cell surface receptor for MERS-CoV has been identified as dipeptidyl peptidase 4 (DPP4), the mouse DPP4 homologue does not allow virus entry into cells. Therefore, development of mouse models of MERS-CoV has been hampered by the fact that MERS-CoV does not replicate in commonly available mouse strains. We have previously described a mouse model in which mDPP4 was replaced with hDPP4 such that hDPP4 is expressed under the endogenous mDPP4 promoter. In this study, we used this mouse model to analyze the host response to MERS-CoV infection using immunological assays and transcriptome analysis. Depletion of CD4+ T cells, CD8+ T cells, or macrophages has no effect on MERS-CoV replication in the lungs of infected mice. However, we found that depletion of CD8+ T cells protects and depletion of macrophages exacerbates MERS-CoV-induced pathology and clinical symptoms of disease. Overall, we demonstrate an important role for the inflammatory response in regulating MERS-CoV pathogenesis in vivo IMPORTANCE: The Middle East respiratory syndrome coronavirus (MERS-CoV) is a highly pathogenic respiratory virus that emerged from zoonotic sources in 2012. Human infections are still occurring throughout Saudi Arabia at a 38% case fatality rate, with the potential for worldwide spread via air travel. In this work, we identify the host response to the virus and identify inflammatory pathways and cell populations that are critical for protection from severe lung disease. By understanding the immune response to MERS-CoV we can develop targeted therapies to inhibit pathogenesis in the future.
DOI: 10.1128/JVI.01825-16
PubMed: 27795435
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Coleman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Sisk, Jeanne M" sort="Sisk, Jeanne M" uniqKey="Sisk J" first="Jeanne M" last="Sisk">Jeanne M. Sisk</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Halasz, Gabor" sort="Halasz, Gabor" uniqKey="Halasz G" first="Gabor" last="Halasz">Gabor Halasz</name><affiliation wicri:level="2"><nlm:affiliation>Regeneron Pharmaceuticals, Tarrytown, New York, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Regeneron Pharmaceuticals, Tarrytown, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Zhong, Jixin" sort="Zhong, Jixin" uniqKey="Zhong J" first="Jixin" last="Zhong">Jixin Zhong</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Beck, Sarah E" sort="Beck, Sarah E" uniqKey="Beck S" first="Sarah E" last="Beck">Sarah E. Beck</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Matthews, Krystal L" sort="Matthews, Krystal L" uniqKey="Matthews K" first="Krystal L" last="Matthews">Krystal L. Matthews</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Venkataraman, Thiagarajan" sort="Venkataraman, Thiagarajan" uniqKey="Venkataraman T" first="Thiagarajan" last="Venkataraman">Thiagarajan Venkataraman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Rajagopalan, Sanjay" sort="Rajagopalan, Sanjay" uniqKey="Rajagopalan S" first="Sanjay" last="Rajagopalan">Sanjay Rajagopalan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Kyratsous, Christos A" sort="Kyratsous, Christos A" uniqKey="Kyratsous C" first="Christos A" last="Kyratsous">Christos A. Kyratsous</name><affiliation wicri:level="2"><nlm:affiliation>Regeneron Pharmaceuticals, Tarrytown, New York, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Regeneron Pharmaceuticals, Tarrytown, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B" last="Frieman">Matthew B. Frieman</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA mfrieman@som.umaryland.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>CD4-Positive T-Lymphocytes (virology)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>CD8-Positive T-Lymphocytes (virology)</term><term>Coronavirus Infections (genetics)</term><term>Coronavirus Infections (immunology)</term><term>Coronavirus Infections (pathology)</term><term>Coronavirus Infections (virology)</term><term>Dipeptidyl Peptidase 4 (genetics)</term><term>Dipeptidyl Peptidase 4 (immunology)</term><term>Disease Models, Animal</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Lung (immunology)</term><term>Lung (virology)</term><term>Lymphocyte Depletion</term><term>Macrophages (immunology)</term><term>Macrophages (virology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Middle East Respiratory Syndrome Coronavirus (genetics)</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term><term>Promoter Regions, Genetic</term><term>Receptors, Virus 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(virologie)</term><term>Lymphocytes T CD8+ (immunologie)</term><term>Lymphocytes T CD8+ (virologie)</term><term>Macrophages (immunologie)</term><term>Macrophages (virologie)</term><term>Modèles animaux de maladie humaine</term><term>Poumon (immunologie)</term><term>Poumon (virologie)</term><term>Pénétration virale</term><term>Récepteurs viraux (génétique)</term><term>Récepteurs viraux (immunologie)</term><term>Régions promotrices (génétique)</term><term>Régulation de l'expression des gènes</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris transgéniques</term><term>Transcriptome</term><term>Transgènes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dipeptidyl Peptidase 4</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Infections à coronavirus</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus Infections</term><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Dipeptidyl peptidase 4</term><term>Infections à coronavirus</term><term>Récepteurs viraux</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Dipeptidyl peptidase 4</term><term>Infections à coronavirus</term><term>Lymphocytes T CD4+</term><term>Lymphocytes T CD8+</term><term>Macrophages</term><term>Poumon</term><term>Récepteurs viraux</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term><term>Coronavirus Infections</term><term>Dipeptidyl Peptidase 4</term><term>Lung</term><term>Macrophages</term><term>Middle East Respiratory Syndrome Coronavirus</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Coronavirus Infections</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term><term>Lymphocytes T CD4+</term><term>Lymphocytes T CD8+</term><term>Macrophages</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term><term>Coronavirus Infections</term><term>Lung</term><term>Macrophages</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Lymphocyte Depletion</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Promoter Regions, Genetic</term><term>Transcriptome</term><term>Transgenes</term><term>Virus Internalization</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Animaux</term><term>Déplétion lymphocytaire</term><term>Humains</term><term>Interactions hôte-pathogène</term><term>Modèles animaux de maladie humaine</term><term>Pénétration virale</term><term>Régions promotrices (génétique)</term><term>Régulation de l'expression des gènes</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris transgéniques</term><term>Transcriptome</term><term>Transgènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Middle East respiratory syndrome coronavirus (MERS-CoV) is an important emerging pathogen that was first described in 2012. While the cell surface receptor for MERS-CoV has been identified as dipeptidyl peptidase 4 (DPP4), the mouse DPP4 homologue does not allow virus entry into cells. Therefore, development of mouse models of MERS-CoV has been hampered by the fact that MERS-CoV does not replicate in commonly available mouse strains. We have previously described a mouse model in which mDPP4 was replaced with hDPP4 such that hDPP4 is expressed under the endogenous mDPP4 promoter. In this study, we used this mouse model to analyze the host response to MERS-CoV infection using immunological assays and transcriptome analysis. Depletion of CD4<sup>+</sup> T cells, CD8<sup>+</sup> T cells, or macrophages has no effect on MERS-CoV replication in the lungs of infected mice. However, we found that depletion of CD8<sup>+</sup> T cells protects and depletion of macrophages exacerbates MERS-CoV-induced pathology and clinical symptoms of disease. Overall, we demonstrate an important role for the inflammatory response in regulating MERS-CoV pathogenesis in vivo IMPORTANCE: The Middle East respiratory syndrome coronavirus (MERS-CoV) is a highly pathogenic respiratory virus that emerged from zoonotic sources in 2012. Human infections are still occurring throughout Saudi Arabia at a 38% case fatality rate, with the potential for worldwide spread via air travel. In this work, we identify the host response to the virus and identify inflammatory pathways and cell populations that are critical for protection from severe lung disease. By understanding the immune response to MERS-CoV we can develop targeted therapies to inhibit pathogenesis in the future.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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