An Acute Immune Response to Middle East Respiratory Syndrome Coronavirus Replication Contributes to Viral Pathogenicity.
Identifieur interne : 001313 ( PubMed/Corpus ); précédent : 001312; suivant : 001314An Acute Immune Response to Middle East Respiratory Syndrome Coronavirus Replication Contributes to Viral Pathogenicity.
Auteurs : Laura J. Baseler ; Darryl Falzarano ; Dana P. Scott ; Rebecca Rosenke ; Tina Thomas ; Vincent J. Munster ; Heinz Feldmann ; Emmie De WitSource :
- The American journal of pathology [ 1525-2191 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Antigens, Viral (analysis), Antigens, Viral (blood), Callithrix, Coronavirus Infections (immunology), Coronavirus Infections (virology), Dipeptidyl Peptidase 4 (metabolism), Disease Models, Animal, Female, Humans, Lung (immunology), Lung (pathology), Macaca mulatta, Macrophages, Alveolar (classification), Male, Middle East Respiratory Syndrome Coronavirus (immunology), Middle East Respiratory Syndrome Coronavirus (pathogenicity), Middle East Respiratory Syndrome Coronavirus (physiology), Neutrophils (immunology), Pneumonia, Viral (immunology), Rabbits, Viral Load, Virulence, Virus Replication (immunology).
- MESH :
- chemical , analysis : Antigens, Viral.
- chemical , blood : Antigens, Viral.
- classification : Macrophages, Alveolar.
- immunology : Coronavirus Infections, Lung, Middle East Respiratory Syndrome Coronavirus, Neutrophils, Pneumonia, Viral, Virus Replication.
- chemical , metabolism : Dipeptidyl Peptidase 4.
- pathogenicity : Middle East Respiratory Syndrome Coronavirus.
- pathology : Lung.
- physiology : Middle East Respiratory Syndrome Coronavirus.
- virology : Coronavirus Infections.
- Animals, Callithrix, Disease Models, Animal, Female, Humans, Macaca mulatta, Male, Rabbits, Viral Load, Virulence.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) was first identified in a human with severe pneumonia in 2012. Since then, infections have been detected in >1500 individuals, with disease severity ranging from asymptomatic to severe, fatal pneumonia. To elucidate the pathogenesis of this virus and investigate mechanisms underlying disease severity variation in the absence of autopsy data, a rhesus macaque and common marmoset model of MERS-CoV disease were analyzed. Rhesus macaques developed mild disease, and common marmosets exhibited moderate to severe, potentially lethal, disease. Both nonhuman primate species exhibited respiratory clinical signs after inoculation, which were more severe and of longer duration in the marmosets, and developed bronchointerstitial pneumonia. In marmosets, the pneumonia was more extensive, with development of severe airway lesions. Quantitative analysis showed significantly higher levels of pulmonary neutrophil infiltration and higher amounts of pulmonary viral antigen in marmosets. Pulmonary expression of the MERS-CoV receptor, dipeptidyl peptidase 4, was similar in marmosets and macaques. These results suggest that increased virus replication and the local immune response to MERS-CoV infection likely play a role in pulmonary pathology severity. Together, the rhesus macaque and common marmoset models of MERS-CoV span the wide range of disease severity reported in MERS-CoV-infected humans, which will aid in investigating MERS-CoV disease pathogenesis.
DOI: 10.1016/j.ajpath.2015.10.025
PubMed: 26724387
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pubmed:26724387Le document en format XML
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Baseler</name><affiliation><nlm:affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana; Department of Comparative Pathobiology, Purdue University, West Lafayette, Indiana.</nlm:affiliation></affiliation></author><author><name sortKey="Falzarano, Darryl" sort="Falzarano, Darryl" uniqKey="Falzarano D" first="Darryl" last="Falzarano">Darryl Falzarano</name><affiliation><nlm:affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</nlm:affiliation></affiliation></author><author><name sortKey="Scott, Dana P" sort="Scott, Dana P" uniqKey="Scott D" first="Dana P" last="Scott">Dana P. Scott</name><affiliation><nlm:affiliation>Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</nlm:affiliation></affiliation></author><author><name sortKey="Rosenke, Rebecca" sort="Rosenke, Rebecca" uniqKey="Rosenke R" first="Rebecca" last="Rosenke">Rebecca Rosenke</name><affiliation><nlm:affiliation>Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</nlm:affiliation></affiliation></author><author><name sortKey="Thomas, Tina" sort="Thomas, Tina" uniqKey="Thomas T" first="Tina" last="Thomas">Tina Thomas</name><affiliation><nlm:affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</nlm:affiliation></affiliation></author><author><name sortKey="Munster, Vincent J" sort="Munster, Vincent J" uniqKey="Munster V" first="Vincent J" last="Munster">Vincent J. 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Electronic address: emmie.dewit@nih.gov.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The American journal of pathology</title><idno type="eISSN">1525-2191</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, Viral (analysis)</term><term>Antigens, Viral (blood)</term><term>Callithrix</term><term>Coronavirus Infections (immunology)</term><term>Coronavirus Infections (virology)</term><term>Dipeptidyl Peptidase 4 (metabolism)</term><term>Disease Models, Animal</term><term>Female</term><term>Humans</term><term>Lung (immunology)</term><term>Lung (pathology)</term><term>Macaca mulatta</term><term>Macrophages, Alveolar (classification)</term><term>Male</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term><term>Middle East Respiratory Syndrome Coronavirus (physiology)</term><term>Neutrophils (immunology)</term><term>Pneumonia, Viral (immunology)</term><term>Rabbits</term><term>Viral Load</term><term>Virulence</term><term>Virus Replication (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antigens, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antigens, Viral</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Macrophages, Alveolar</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus Infections</term><term>Lung</term><term>Middle East Respiratory Syndrome Coronavirus</term><term>Neutrophils</term><term>Pneumonia, Viral</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dipeptidyl Peptidase 4</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Disease Models, Animal</term><term>Female</term><term>Humans</term><term>Macaca mulatta</term><term>Male</term><term>Rabbits</term><term>Viral Load</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Middle East respiratory syndrome coronavirus (MERS-CoV) was first identified in a human with severe pneumonia in 2012. Since then, infections have been detected in >1500 individuals, with disease severity ranging from asymptomatic to severe, fatal pneumonia. To elucidate the pathogenesis of this virus and investigate mechanisms underlying disease severity variation in the absence of autopsy data, a rhesus macaque and common marmoset model of MERS-CoV disease were analyzed. Rhesus macaques developed mild disease, and common marmosets exhibited moderate to severe, potentially lethal, disease. Both nonhuman primate species exhibited respiratory clinical signs after inoculation, which were more severe and of longer duration in the marmosets, and developed bronchointerstitial pneumonia. In marmosets, the pneumonia was more extensive, with development of severe airway lesions. Quantitative analysis showed significantly higher levels of pulmonary neutrophil infiltration and higher amounts of pulmonary viral antigen in marmosets. Pulmonary expression of the MERS-CoV receptor, dipeptidyl peptidase 4, was similar in marmosets and macaques. These results suggest that increased virus replication and the local immune response to MERS-CoV infection likely play a role in pulmonary pathology severity. Together, the rhesus macaque and common marmoset models of MERS-CoV span the wide range of disease severity reported in MERS-CoV-infected humans, which will aid in investigating MERS-CoV disease pathogenesis. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26724387</PMID><DateCompleted><Year>2016</Year><Month>08</Month><Day>09</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-2191</ISSN><JournalIssue CitedMedium="Internet"><Volume>186</Volume><Issue>3</Issue><PubDate><Year>2016</Year><Month>Mar</Month></PubDate></JournalIssue><Title>The American journal of pathology</Title><ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>An Acute Immune Response to Middle East Respiratory Syndrome Coronavirus Replication Contributes to Viral Pathogenicity.</ArticleTitle><Pagination><MedlinePgn>630-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ajpath.2015.10.025</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0002-9440(15)00649-5</ELocationID><Abstract><AbstractText>Middle East respiratory syndrome coronavirus (MERS-CoV) was first identified in a human with severe pneumonia in 2012. Since then, infections have been detected in >1500 individuals, with disease severity ranging from asymptomatic to severe, fatal pneumonia. To elucidate the pathogenesis of this virus and investigate mechanisms underlying disease severity variation in the absence of autopsy data, a rhesus macaque and common marmoset model of MERS-CoV disease were analyzed. Rhesus macaques developed mild disease, and common marmosets exhibited moderate to severe, potentially lethal, disease. Both nonhuman primate species exhibited respiratory clinical signs after inoculation, which were more severe and of longer duration in the marmosets, and developed bronchointerstitial pneumonia. In marmosets, the pneumonia was more extensive, with development of severe airway lesions. Quantitative analysis showed significantly higher levels of pulmonary neutrophil infiltration and higher amounts of pulmonary viral antigen in marmosets. Pulmonary expression of the MERS-CoV receptor, dipeptidyl peptidase 4, was similar in marmosets and macaques. These results suggest that increased virus replication and the local immune response to MERS-CoV infection likely play a role in pulmonary pathology severity. Together, the rhesus macaque and common marmoset models of MERS-CoV span the wide range of disease severity reported in MERS-CoV-infected humans, which will aid in investigating MERS-CoV disease pathogenesis. </AbstractText><CopyrightInformation>Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baseler</LastName><ForeName>Laura J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana; Department of Comparative Pathobiology, Purdue University, West Lafayette, Indiana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Falzarano</LastName><ForeName>Darryl</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scott</LastName><ForeName>Dana P</ForeName><Initials>DP</Initials><AffiliationInfo><Affiliation>Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosenke</LastName><ForeName>Rebecca</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>Tina</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Munster</LastName><ForeName>Vincent J</ForeName><Initials>VJ</Initials><AffiliationInfo><Affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feldmann</LastName><ForeName>Heinz</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Wit</LastName><ForeName>Emmie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, Rocky Mountain Laboratories, Hamilton, Montana. Electronic address: emmie.dewit@nih.gov.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>12</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Pathol</MedlineTA><NlmUniqueID>0370502</NlmUniqueID><ISSNLinking>0002-9440</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000956">Antigens, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.14.5</RegistryNumber><NameOfSubstance UI="D018819">Dipeptidyl Peptidase 4</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000956" MajorTopicYN="N">Antigens, Viral</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002144" MajorTopicYN="N">Callithrix</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018819" MajorTopicYN="N">Dipeptidyl Peptidase 4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">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="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008253" MajorTopicYN="N">Macaca mulatta</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016676" MajorTopicYN="N">Macrophages, Alveolar</DescriptorName><QualifierName UI="Q000145" MajorTopicYN="N">classification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D065207" MajorTopicYN="N">Middle East Respiratory Syndrome Coronavirus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009504" MajorTopicYN="N">Neutrophils</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014774" 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