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Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice.

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Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice.

Auteurs : Kun Li [États-Unis] ; Christine L. Wohlford-Lenane [États-Unis] ; Rudragouda Channappanavar [États-Unis] ; Jung-Eun Park [États-Unis] ; James T. Earnest [États-Unis] ; Thomas B. Bair [États-Unis] ; Amber M. Bates [États-Unis] ; Kim A. Brogden [États-Unis] ; Heather A. Flaherty [États-Unis] ; Tom Gallagher [États-Unis] ; David K. Meyerholz [États-Unis] ; Stanley Perlman [États-Unis] ; Paul B. Mccray [États-Unis]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2017.

RBID : pubmed:28348219

Descripteurs français

KwdFr :
- Animaux, Coronavirus du syndrome respiratoire du Moyen-Orient (génétique), Dipeptidyl peptidase 4 (génétique), Dipeptidyl peptidase 4 (métabolisme), Femelle, Glycoprotéine de spicule des coronavirus (génétique), Humains, Infections à coronavirus (), Infections à coronavirus (virologie), Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (métabolisme), Maladies pulmonaires (étiologie), Modèles animaux de maladie humaine, Mutation, Mâle, Réplication virale, Souris, Souris de lignée C57BL.
MESH :
- anatomopathologie : Maladies pulmonaires.
- génétique : Coronavirus du syndrome respiratoire du Moyen-Orient, Dipeptidyl peptidase 4, Glycoprotéine de spicule des coronavirus.
- métabolisme : Dipeptidyl peptidase 4, Maladies pulmonaires.
- virologie : Infections à coronavirus.
- étiologie : Maladies pulmonaires.
- Animaux, Femelle, Humains, Infections à coronavirus, Modèles animaux de maladie humaine, Mutation, Mâle, Réplication virale, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- Animals, Coronavirus Infections (complications), Coronavirus Infections (virology), Dipeptidyl Peptidase 4 (genetics), Dipeptidyl Peptidase 4 (metabolism), Disease Models, Animal, Female, Humans, Lung Diseases (etiology), Lung Diseases (metabolism), Lung Diseases (pathology), Male, Mice, Mice, Inbred C57BL, Middle East Respiratory Syndrome Coronavirus (genetics), Mutation, Spike Glycoprotein, Coronavirus (genetics), Virus Replication.
MESH :
- chemical , genetics : Dipeptidyl Peptidase 4, Spike Glycoprotein, Coronavirus.
- complications : Coronavirus Infections.
- etiology : Lung Diseases.
- genetics : Middle East Respiratory Syndrome Coronavirus.
- chemical , metabolism : Dipeptidyl Peptidase 4, Lung Diseases.
- pathology : Lung Diseases.
- virology : Coronavirus Infections.
- Animals, Disease Models, Animal, Female, Humans, Male, Mice, Mice, Inbred C57BL, Mutation, Virus Replication.

Abstract

The Middle East respiratory syndrome (MERS) emerged in Saudi Arabia in 2012, caused by a zoonotically transmitted coronavirus (CoV). Over 1,900 cases have been reported to date, with ∼36% fatality rate. Lack of autopsies from MERS cases has hindered understanding of MERS-CoV pathogenesis. A small animal model that develops progressive pulmonary manifestations when infected with MERS-CoV would advance the field. As mice are restricted to infection at the level of DPP4, the MERS-CoV receptor, we generated mice with humanized exons 10-12 of the mouse Dpp4 locus. Upon inoculation with MERS-CoV, human DPP4 knockin (KI) mice supported virus replication in the lungs, but developed no illness. After 30 serial passages through the lungs of KI mice, a mouse-adapted virus emerged (MERS_MA) that grew in lungs to over 100 times higher titers than the starting virus. A plaque-purified MERS_MA clone caused weight loss and fatal infection. Virus antigen was observed in airway epithelia, pneumocytes, and macrophages. Pathologic findings included diffuse alveolar damage with pulmonary edema and hyaline membrane formation associated with accumulation of activated inflammatory monocyte-macrophages and neutrophils in the lungs. Relative to the parental MERS-CoV, MERS_MA viruses contained 13-22 mutations, including several within the spike (S) glycoprotein gene. S-protein mutations sensitized viruses to entry-activating serine proteases and conferred more rapid entry kinetics. Recombinant MERS_MA bearing mutant S proteins were more virulent than the parental virus in hDPP4 KI mice. The hDPP4 KI mouse and the MERS_MA provide tools to investigate disease causes and develop new therapies.

DOI: 10.1073/pnas.1619109114
PubMed: 28348219

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<term>Dipeptidyl peptidase 4</term>
<term>Glycoprotéine de spicule des coronavirus</term>
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<front><div type="abstract" xml:lang="en">The Middle East respiratory syndrome (MERS) emerged in Saudi Arabia in 2012, caused by a zoonotically transmitted coronavirus (CoV). Over 1,900 cases have been reported to date, with ∼36% fatality rate. Lack of autopsies from MERS cases has hindered understanding of MERS-CoV pathogenesis. A small animal model that develops progressive pulmonary manifestations when infected with MERS-CoV would advance the field. As mice are restricted to infection at the level of DPP4, the MERS-CoV receptor, we generated mice with humanized exons 10-12 of the mouse <i>Dpp4</i>
 locus. Upon inoculation with MERS-CoV, human DPP4 knockin (KI) mice supported virus replication in the lungs, but developed no illness. After 30 serial passages through the lungs of KI mice, a mouse-adapted virus emerged (MERS<sub>MA</sub>
) that grew in lungs to over 100 times higher titers than the starting virus. A plaque-purified MERS<sub>MA</sub>
 clone caused weight loss and fatal infection. Virus antigen was observed in airway epithelia, pneumocytes, and macrophages. Pathologic findings included diffuse alveolar damage with pulmonary edema and hyaline membrane formation associated with accumulation of activated inflammatory monocyte-macrophages and neutrophils in the lungs. Relative to the parental MERS-CoV, MERS<sub>MA</sub>
 viruses contained 13-22 mutations, including several within the spike (S) glycoprotein gene. S-protein mutations sensitized viruses to entry-activating serine proteases and conferred more rapid entry kinetics. Recombinant MERS<sub>MA</sub>
 bearing mutant S proteins were more virulent than the parental virus in hDPP4 KI mice. The hDPP4 KI mouse and the MERS<sub>MA</sub>
 provide tools to investigate disease causes and develop new therapies.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28348219</PMID>
<DateCompleted><Year>2018</Year>
<Month>05</Month>
<Day>17</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>114</Volume>
<Issue>15</Issue>
<PubDate><Year>2017</Year>
<Month>04</Month>
<Day>11</Day>
</PubDate>
</JournalIssue>
<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
<ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation>
</Journal>
<ArticleTitle>Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice.</ArticleTitle>
<Pagination><MedlinePgn>E3119-E3128</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1619109114</ELocationID>
<Abstract><AbstractText>The Middle East respiratory syndrome (MERS) emerged in Saudi Arabia in 2012, caused by a zoonotically transmitted coronavirus (CoV). Over 1,900 cases have been reported to date, with ∼36% fatality rate. Lack of autopsies from MERS cases has hindered understanding of MERS-CoV pathogenesis. A small animal model that develops progressive pulmonary manifestations when infected with MERS-CoV would advance the field. As mice are restricted to infection at the level of DPP4, the MERS-CoV receptor, we generated mice with humanized exons 10-12 of the mouse <i>Dpp4</i>
 locus. Upon inoculation with MERS-CoV, human DPP4 knockin (KI) mice supported virus replication in the lungs, but developed no illness. After 30 serial passages through the lungs of KI mice, a mouse-adapted virus emerged (MERS<sub>MA</sub>
) that grew in lungs to over 100 times higher titers than the starting virus. A plaque-purified MERS<sub>MA</sub>
 clone caused weight loss and fatal infection. Virus antigen was observed in airway epithelia, pneumocytes, and macrophages. Pathologic findings included diffuse alveolar damage with pulmonary edema and hyaline membrane formation associated with accumulation of activated inflammatory monocyte-macrophages and neutrophils in the lungs. Relative to the parental MERS-CoV, MERS<sub>MA</sub>
 viruses contained 13-22 mutations, including several within the spike (S) glycoprotein gene. S-protein mutations sensitized viruses to entry-activating serine proteases and conferred more rapid entry kinetics. Recombinant MERS<sub>MA</sub>
 bearing mutant S proteins were more virulent than the parental virus in hDPP4 KI mice. The hDPP4 KI mouse and the MERS<sub>MA</sub>
 provide tools to investigate disease causes and develop new therapies.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Kun</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Pappajohn Biomedical Institute, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wohlford-Lenane</LastName>
<ForeName>Christine L</ForeName>
<Initials>CL</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Pappajohn Biomedical Institute, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Channappanavar</LastName>
<ForeName>Rudragouda</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Park</LastName>
<ForeName>Jung-Eun</ForeName>
<Initials>JE</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Loyola University Chicago, Maywood, IL 60153.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Earnest</LastName>
<ForeName>James T</ForeName>
<Initials>JT</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Loyola University Chicago, Maywood, IL 60153.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bair</LastName>
<ForeName>Thomas B</ForeName>
<Initials>TB</Initials>
<AffiliationInfo><Affiliation>Iowa Institute of Human Genetics, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bates</LastName>
<ForeName>Amber M</ForeName>
<Initials>AM</Initials>
<AffiliationInfo><Affiliation>College of Dentistry, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Brogden</LastName>
<ForeName>Kim A</ForeName>
<Initials>KA</Initials>
<AffiliationInfo><Affiliation>College of Dentistry, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Flaherty</LastName>
<ForeName>Heather A</ForeName>
<Initials>HA</Initials>
<AffiliationInfo><Affiliation>Department of Veterinary Pathology, Iowa State University, Ames, IA 50011.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gallagher</LastName>
<ForeName>Tom</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Loyola University Chicago, Maywood, IL 60153.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Meyerholz</LastName>
<ForeName>David K</ForeName>
<Initials>DK</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Perlman</LastName>
<ForeName>Stanley</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Pappajohn Biomedical Institute, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>McCray</LastName>
<ForeName>Paul B</ForeName>
<Initials>PB</Initials>
<Suffix>Jr</Suffix>
<AffiliationInfo><Affiliation>Department of Pediatrics, Pappajohn Biomedical Institute, University of Iowa, Iowa City, IA 52242; paul-mccray@uiowa.edu.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Iowa, Iowa City, IA 52242.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P01 AI060699</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 DK054759</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 ES005605</GrantID>
<Acronym>ES</Acronym>
<Agency>NIEHS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T90 DE023520</GrantID>
<Acronym>DE</Acronym>
<Agency>NIDCR NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>03</Month>
<Day>27</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Proc Natl Acad Sci U S A</MedlineTA>
<NlmUniqueID>7505876</NlmUniqueID>
<ISSNLinking>0027-8424</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D064370">Spike Glycoprotein, Coronavirus</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>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="Y">complications</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="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008171" MajorTopicYN="N">Lung Diseases</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D065207" MajorTopicYN="N">Middle East Respiratory Syndrome Coronavirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="Y">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064370" MajorTopicYN="N">Spike Glycoprotein, Coronavirus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">CD26</Keyword>
<Keyword MajorTopicYN="Y">emerging pathogen</Keyword>
<Keyword MajorTopicYN="Y">interferon</Keyword>
<Keyword MajorTopicYN="Y">spike protein</Keyword>
<Keyword MajorTopicYN="Y">virus pathogenesis</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>3</Month>
<Day>30</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2018</Year>
<Month>5</Month>
<Day>18</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>3</Month>
<Day>29</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice.

Mouse-adapted MERS coronavirus causes lethal lung disease in human DPP4 knockin mice.

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