Lack of innate interferon responses during SARS coronavirus infection in a vaccination and reinfection ferret model.
Identifieur interne : 001300 ( PubMed/Corpus ); précédent : 001299; suivant : 001301Lack of innate interferon responses during SARS coronavirus infection in a vaccination and reinfection ferret model.
Auteurs : Mark J. Cameron ; Alyson A. Kelvin ; Alberto J. Leon ; Cheryl M. Cameron ; Longsi Ran ; Luoling Xu ; Yong-Kyu Chu ; Ali Danesh ; Yuan Fang ; Qianjun Li ; Austin Anderson ; Ronald C. Couch ; Stephane G. Paquette ; Ndingsa G. Fomukong ; Otfried Kistner ; Manfred Lauchart ; Thomas Rowe ; Kevin S. Harrod ; Colleen B. Jonsson ; David J. KelvinSource :
- PloS one [ 1932-6203 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Antibodies, Viral (blood), Chlorocebus aethiops, Complement System Proteins (genetics), Complement System Proteins (metabolism), Ferrets, Gene Expression Regulation, Host-Pathogen Interactions, Immunity, Innate, Interferons (genetics), Interferons (metabolism), Interleukin-6 (genetics), Interleukin-6 (metabolism), Lung (metabolism), Lung (virology), Male, Oligonucleotide Array Sequence Analysis, SARS Virus (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (prevention & control), Transcriptome, Vaccination, Vero Cells, Viral Load, Viral Vaccines (administration & dosage).
- MESH :
- chemical , administration & dosage : Viral Vaccines.
- chemical , blood : Antibodies, Viral.
- chemical , genetics : Complement System Proteins, Interferons, Interleukin-6.
- chemical , metabolism : Complement System Proteins, Interferons, Interleukin-6.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- metabolism : Lung, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- prevention & control : Severe Acute Respiratory Syndrome.
- virology : Lung.
- Animals, Chlorocebus aethiops, Ferrets, Gene Expression Regulation, Host-Pathogen Interactions, Immunity, Innate, Male, Oligonucleotide Array Sequence Analysis, Transcriptome, Vaccination, Vero Cells, Viral Load.
Abstract
In terms of its highly pathogenic nature, there remains a significant need to further define the immune pathology of SARS-coronavirus (SARS-CoV) infection, as well as identify correlates of immunity to help develop vaccines for severe coronaviral infections. Here we use a SARS-CoV infection-reinfection ferret model and a functional genomics approach to gain insight into SARS immunopathogenesis and to identify correlates of immune protection during SARS-CoV-challenge in ferrets previously infected with SARS-CoV or immunized with a SARS virus vaccine. We identified gene expression signatures in the lungs of ferrets associated with primary immune responses to SARS-CoV infection and in ferrets that received an identical second inoculum. Acute SARS-CoV infection prompted coordinated innate immune responses that were dominated by antiviral IFN response gene (IRG) expression. Reinfected ferrets, however, lacked the integrated expression of IRGs that was prevalent during acute infection. The expression of specific IRGs was also absent upon challenge in ferrets immunized with an inactivated, Al(OH)(3)-adjuvanted whole virus SARS vaccine candidate that protected them against SARS-CoV infection in the lungs. Lack of IFN-mediated immune enhancement in infected ferrets that were previously inoculated with, or vaccinated against, SARS-CoV revealed 9 IRG correlates of protective immunity. This data provides insight into the molecular pathogenesis of SARS-CoV and SARS-like-CoV infections and is an important resource for the development of CoV antiviral therapeutics and vaccines.
DOI: 10.1371/journal.pone.0045842
PubMed: 23029269
Links to Exploration step
pubmed:23029269Le document en format XML
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Cameron</name><affiliation><nlm:affiliation>Division of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Kelvin, Alyson A" sort="Kelvin, Alyson A" uniqKey="Kelvin A" first="Alyson A" last="Kelvin">Alyson A. Kelvin</name></author><author><name sortKey="Leon, Alberto J" sort="Leon, Alberto J" uniqKey="Leon A" first="Alberto J" last="Leon">Alberto J. Leon</name></author><author><name sortKey="Cameron, Cheryl M" sort="Cameron, Cheryl M" uniqKey="Cameron C" first="Cheryl M" last="Cameron">Cheryl M. Cameron</name></author><author><name sortKey="Ran, Longsi" sort="Ran, Longsi" uniqKey="Ran L" first="Longsi" last="Ran">Longsi Ran</name></author><author><name sortKey="Xu, Luoling" sort="Xu, Luoling" uniqKey="Xu L" first="Luoling" last="Xu">Luoling Xu</name></author><author><name sortKey="Chu, Yong Kyu" sort="Chu, Yong Kyu" uniqKey="Chu Y" first="Yong-Kyu" last="Chu">Yong-Kyu Chu</name></author><author><name sortKey="Danesh, Ali" sort="Danesh, Ali" uniqKey="Danesh A" first="Ali" last="Danesh">Ali Danesh</name></author><author><name sortKey="Fang, Yuan" sort="Fang, Yuan" uniqKey="Fang Y" first="Yuan" last="Fang">Yuan Fang</name></author><author><name sortKey="Li, Qianjun" sort="Li, Qianjun" uniqKey="Li Q" first="Qianjun" last="Li">Qianjun Li</name></author><author><name sortKey="Anderson, Austin" sort="Anderson, Austin" uniqKey="Anderson A" first="Austin" last="Anderson">Austin Anderson</name></author><author><name sortKey="Couch, Ronald C" sort="Couch, Ronald C" uniqKey="Couch R" first="Ronald C" last="Couch">Ronald C. 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Harrod</name></author><author><name sortKey="Jonsson, Colleen B" sort="Jonsson, Colleen B" uniqKey="Jonsson C" first="Colleen B" last="Jonsson">Colleen B. Jonsson</name></author><author><name sortKey="Kelvin, David J" sort="Kelvin, David J" uniqKey="Kelvin D" first="David J" last="Kelvin">David J. Kelvin</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Viral (blood)</term><term>Chlorocebus aethiops</term><term>Complement System Proteins (genetics)</term><term>Complement System Proteins (metabolism)</term><term>Ferrets</term><term>Gene Expression Regulation</term><term>Host-Pathogen Interactions</term><term>Immunity, Innate</term><term>Interferons (genetics)</term><term>Interferons (metabolism)</term><term>Interleukin-6 (genetics)</term><term>Interleukin-6 (metabolism)</term><term>Lung (metabolism)</term><term>Lung (virology)</term><term>Male</term><term>Oligonucleotide Array Sequence Analysis</term><term>SARS Virus (immunology)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Severe Acute Respiratory Syndrome (prevention & control)</term><term>Transcriptome</term><term>Vaccination</term><term>Vero Cells</term><term>Viral Load</term><term>Viral Vaccines (administration & dosage)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Viral Vaccines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antibodies, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Complement System Proteins</term><term>Interferons</term><term>Interleukin-6</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Complement System Proteins</term><term>Interferons</term><term>Interleukin-6</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chlorocebus aethiops</term><term>Ferrets</term><term>Gene Expression Regulation</term><term>Host-Pathogen Interactions</term><term>Immunity, Innate</term><term>Male</term><term>Oligonucleotide Array Sequence Analysis</term><term>Transcriptome</term><term>Vaccination</term><term>Vero Cells</term><term>Viral Load</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In terms of its highly pathogenic nature, there remains a significant need to further define the immune pathology of SARS-coronavirus (SARS-CoV) infection, as well as identify correlates of immunity to help develop vaccines for severe coronaviral infections. Here we use a SARS-CoV infection-reinfection ferret model and a functional genomics approach to gain insight into SARS immunopathogenesis and to identify correlates of immune protection during SARS-CoV-challenge in ferrets previously infected with SARS-CoV or immunized with a SARS virus vaccine. We identified gene expression signatures in the lungs of ferrets associated with primary immune responses to SARS-CoV infection and in ferrets that received an identical second inoculum. Acute SARS-CoV infection prompted coordinated innate immune responses that were dominated by antiviral IFN response gene (IRG) expression. Reinfected ferrets, however, lacked the integrated expression of IRGs that was prevalent during acute infection. The expression of specific IRGs was also absent upon challenge in ferrets immunized with an inactivated, Al(OH)(3)-adjuvanted whole virus SARS vaccine candidate that protected them against SARS-CoV infection in the lungs. Lack of IFN-mediated immune enhancement in infected ferrets that were previously inoculated with, or vaccinated against, SARS-CoV revealed 9 IRG correlates of protective immunity. This data provides insight into the molecular pathogenesis of SARS-CoV and SARS-like-CoV infections and is an important resource for the development of CoV antiviral therapeutics and vaccines.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23029269</PMID><DateCompleted><Year>2013</Year><Month>02</Month><Day>28</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>9</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Lack of innate interferon responses during SARS coronavirus infection in a vaccination and reinfection ferret model.</ArticleTitle><Pagination><MedlinePgn>e45842</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0045842</ELocationID><Abstract><AbstractText>In terms of its highly pathogenic nature, there remains a significant need to further define the immune pathology of SARS-coronavirus (SARS-CoV) infection, as well as identify correlates of immunity to help develop vaccines for severe coronaviral infections. Here we use a SARS-CoV infection-reinfection ferret model and a functional genomics approach to gain insight into SARS immunopathogenesis and to identify correlates of immune protection during SARS-CoV-challenge in ferrets previously infected with SARS-CoV or immunized with a SARS virus vaccine. We identified gene expression signatures in the lungs of ferrets associated with primary immune responses to SARS-CoV infection and in ferrets that received an identical second inoculum. Acute SARS-CoV infection prompted coordinated innate immune responses that were dominated by antiviral IFN response gene (IRG) expression. Reinfected ferrets, however, lacked the integrated expression of IRGs that was prevalent during acute infection. The expression of specific IRGs was also absent upon challenge in ferrets immunized with an inactivated, Al(OH)(3)-adjuvanted whole virus SARS vaccine candidate that protected them against SARS-CoV infection in the lungs. Lack of IFN-mediated immune enhancement in infected ferrets that were previously inoculated with, or vaccinated against, SARS-CoV revealed 9 IRG correlates of protective immunity. This data provides insight into the molecular pathogenesis of SARS-CoV and SARS-like-CoV infections and is an important resource for the development of CoV antiviral therapeutics and vaccines.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cameron</LastName><ForeName>Mark J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Division of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kelvin</LastName><ForeName>Alyson A</ForeName><Initials>AA</Initials></Author><Author ValidYN="Y"><LastName>Leon</LastName><ForeName>Alberto J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Cameron</LastName><ForeName>Cheryl M</ForeName><Initials>CM</Initials></Author><Author ValidYN="Y"><LastName>Ran</LastName><ForeName>Longsi</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Luoling</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Chu</LastName><ForeName>Yong-Kyu</ForeName><Initials>YK</Initials></Author><Author ValidYN="Y"><LastName>Danesh</LastName><ForeName>Ali</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Fang</LastName><ForeName>Yuan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Qianjun</ForeName><Initials>Q</Initials></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Austin</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Couch</LastName><ForeName>Ronald C</ForeName><Initials>RC</Initials></Author><Author ValidYN="Y"><LastName>Paquette</LastName><ForeName>Stephane G</ForeName><Initials>SG</Initials></Author><Author ValidYN="Y"><LastName>Fomukong</LastName><ForeName>Ndingsa G</ForeName><Initials>NG</Initials></Author><Author ValidYN="Y"><LastName>Kistner</LastName><ForeName>Otfried</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Lauchart</LastName><ForeName>Manfred</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Rowe</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Harrod</LastName><ForeName>Kevin S</ForeName><Initials>KS</Initials></Author><Author ValidYN="Y"><LastName>Jonsson</LastName><ForeName>Colleen B</ForeName><Initials>CB</Initials></Author><Author ValidYN="Y"><LastName>Kelvin</LastName><ForeName>David J</ForeName><Initials>DJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01-AI-30063</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal 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MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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