CD8+ T Cells and Macrophages Regulate Pathogenesis in a Mouse Model of Middle East Respiratory Syndrome.
Identifieur interne : 000D75 ( PubMed/Checkpoint ); précédent : 000D74; suivant : 000D76CD8+ T Cells and Macrophages Regulate Pathogenesis in a Mouse Model of Middle East Respiratory Syndrome.
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
Affiliations:
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<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 (genetics)</term>
<term>Receptors, Virus (immunology)</term>
<term>Transcriptome</term>
<term>Transgenes</term>
<term>Virus Internalization</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Coronavirus du syndrome respiratoire du Moyen-Orient (génétique)</term>
<term>Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie)</term>
<term>Coronavirus du syndrome respiratoire du Moyen-Orient (pathogénicité)</term>
<term>Dipeptidyl peptidase 4 (génétique)</term>
<term>Dipeptidyl peptidase 4 (immunologie)</term>
<term>Déplétion lymphocytaire</term>
<term>Humains</term>
<term>Infections à coronavirus (anatomopathologie)</term>
<term>Infections à coronavirus (génétique)</term>
<term>Infections à coronavirus (immunologie)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Interactions hôte-pathogène</term>
<term>Lymphocytes T CD4+ (immunologie)</term>
<term>Lymphocytes T CD4+ (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>
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<term>Régulation de l'expression des gènes</term>
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<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>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27795435</PMID>
<DateCompleted><Year>2017</Year>
<Month>05</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>06</Month>
<Day>15</Day>
</DateRevised>
<Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>91</Volume>
<Issue>1</Issue>
<PubDate><Year>2017</Year>
<Month>Jan</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Journal of virology</Title>
<ISOAbbreviation>J. Virol.</ISOAbbreviation>
</Journal>
<ArticleTitle>CD8+ T Cells and Macrophages Regulate Pathogenesis in a Mouse Model of Middle East Respiratory Syndrome.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">e01825-16</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01825-16</ELocationID>
<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Copyright © 2016 American Society for Microbiology.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Coleman</LastName>
<ForeName>Christopher M</ForeName>
<Initials>CM</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sisk</LastName>
<ForeName>Jeanne M</ForeName>
<Initials>JM</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Halasz</LastName>
<ForeName>Gabor</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Regeneron Pharmaceuticals, Tarrytown, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhong</LastName>
<ForeName>Jixin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Beck</LastName>
<ForeName>Sarah E</ForeName>
<Initials>SE</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Matthews</LastName>
<ForeName>Krystal L</ForeName>
<Initials>KL</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Venkataraman</LastName>
<ForeName>Thiagarajan</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rajagopalan</LastName>
<ForeName>Sanjay</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kyratsous</LastName>
<ForeName>Christos A</ForeName>
<Initials>CA</Initials>
<AffiliationInfo><Affiliation>Regeneron Pharmaceuticals, Tarrytown, New York, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Frieman</LastName>
<ForeName>Matthew B</ForeName>
<Initials>MB</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA mfrieman@som.umaryland.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>F32 AI118303</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AI095569</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL127422</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>K01 OD021323</GrantID>
<Acronym>OD</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 AI095190</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>12</Month>
<Day>16</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Virol</MedlineTA>
<NlmUniqueID>0113724</NlmUniqueID>
<ISSNLinking>0022-538X</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="C042807">DPP4 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="D018819">Dipeptidyl Peptidase 4</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber>
<NameOfSubstance UI="C545245">Dpp4 protein, mouse</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018819" MajorTopicYN="N">Dipeptidyl Peptidase 4</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008212" MajorTopicYN="N">Lymphocyte Depletion</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D065207" MajorTopicYN="N">Middle East Respiratory Syndrome Coronavirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019076" MajorTopicYN="N">Transgenes</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053586" MajorTopicYN="N">Virus Internalization</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">DPP4</Keyword>
<Keyword MajorTopicYN="Y">MERS</Keyword>
<Keyword MajorTopicYN="Y">MERS-CoV</Keyword>
<Keyword MajorTopicYN="Y">coronavirus</Keyword>
<Keyword MajorTopicYN="Y">immune response</Keyword>
<Keyword MajorTopicYN="Y">mouse model</Keyword>
<Keyword MajorTopicYN="Y">pathogenesis</Keyword>
<Keyword MajorTopicYN="Y">viral pathogenesis</Keyword>
</KeywordList>
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