Early upregulation of acute respiratory distress syndrome-associated cytokines promotes lethal disease in an aged-mouse model of severe acute respiratory syndrome coronavirus infection.
Identifieur interne : 000745 ( PubMed/Corpus ); précédent : 000744; suivant : 000746Early upregulation of acute respiratory distress syndrome-associated cytokines promotes lethal disease in an aged-mouse model of severe acute respiratory syndrome coronavirus infection.
Auteurs : Barry Rockx ; Tracey Baas ; Gregory A. Zornetzer ; Bart Haagmans ; Timothy Sheahan ; Matthew Frieman ; Matthew D. Dyer ; Thomas H. Teal ; Sean Proll ; Judith Van Den Brand ; Ralph Baric ; Michael G. KatzeSource :
- Journal of virology [ 1098-5514 ] ; 2009.
English descriptors
- KwdEn :
- Aging (immunology), Animals, Cytokines (genetics), Cytokines (immunology), Death, Disease Models, Animal, Female, Gene Expression, Humans, Lung (immunology), Lung (pathology), Membrane Glycoproteins (immunology), Mice, Mice, Inbred BALB C, Respiratory Distress Syndrome, Adult (genetics), Respiratory Distress Syndrome, Adult (immunology), Respiratory Distress Syndrome, Adult (mortality), Respiratory Distress Syndrome, Adult (virology), SARS Virus (immunology), SARS Virus (isolation & purification), SARS Virus (physiology), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Spike Glycoprotein, Coronavirus, Up-Regulation, Viral Envelope Proteins (immunology).
- MESH :
- chemical , genetics : Cytokines.
- complications : Severe Acute Respiratory Syndrome.
- genetics : Respiratory Distress Syndrome, Adult, Severe Acute Respiratory Syndrome.
- immunology : Aging, Cytokines, Lung, Membrane Glycoproteins, Respiratory Distress Syndrome, Adult, SARS Virus, Severe Acute Respiratory Syndrome, Viral Envelope Proteins.
- isolation & purification : SARS Virus.
- mortality : Respiratory Distress Syndrome, Adult.
- pathology : Lung.
- physiology : SARS Virus.
- virology : Respiratory Distress Syndrome, Adult, Severe Acute Respiratory Syndrome.
- Animals, Death, Disease Models, Animal, Female, Gene Expression, Humans, Mice, Mice, Inbred BALB C, Spike Glycoprotein, Coronavirus, Up-Regulation.
Abstract
Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.
DOI: 10.1128/JVI.00127-09
PubMed: 19420084
Links to Exploration step
pubmed:19420084Le document en format XML
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Zornetzer</name></author><author><name sortKey="Haagmans, Bart" sort="Haagmans, Bart" uniqKey="Haagmans B" first="Bart" last="Haagmans">Bart Haagmans</name></author><author><name sortKey="Sheahan, Timothy" sort="Sheahan, Timothy" uniqKey="Sheahan T" first="Timothy" last="Sheahan">Timothy Sheahan</name></author><author><name sortKey="Frieman, Matthew" sort="Frieman, Matthew" uniqKey="Frieman M" first="Matthew" last="Frieman">Matthew Frieman</name></author><author><name sortKey="Dyer, Matthew D" sort="Dyer, Matthew D" uniqKey="Dyer M" first="Matthew D" last="Dyer">Matthew D. Dyer</name></author><author><name sortKey="Teal, Thomas H" sort="Teal, Thomas H" uniqKey="Teal T" first="Thomas H" last="Teal">Thomas H. 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Zornetzer</name></author><author><name sortKey="Haagmans, Bart" sort="Haagmans, Bart" uniqKey="Haagmans B" first="Bart" last="Haagmans">Bart Haagmans</name></author><author><name sortKey="Sheahan, Timothy" sort="Sheahan, Timothy" uniqKey="Sheahan T" first="Timothy" last="Sheahan">Timothy Sheahan</name></author><author><name sortKey="Frieman, Matthew" sort="Frieman, Matthew" uniqKey="Frieman M" first="Matthew" last="Frieman">Matthew Frieman</name></author><author><name sortKey="Dyer, Matthew D" sort="Dyer, Matthew D" uniqKey="Dyer M" first="Matthew D" last="Dyer">Matthew D. Dyer</name></author><author><name sortKey="Teal, Thomas H" sort="Teal, Thomas H" uniqKey="Teal T" first="Thomas H" last="Teal">Thomas H. Teal</name></author><author><name sortKey="Proll, Sean" sort="Proll, Sean" uniqKey="Proll S" first="Sean" last="Proll">Sean Proll</name></author><author><name sortKey="Van Den Brand, Judith" sort="Van Den Brand, Judith" uniqKey="Van Den Brand J" first="Judith" last="Van Den Brand">Judith Van Den Brand</name></author><author><name sortKey="Baric, Ralph" sort="Baric, Ralph" uniqKey="Baric R" first="Ralph" last="Baric">Ralph Baric</name></author><author><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (immunology)</term><term>Animals</term><term>Cytokines (genetics)</term><term>Cytokines (immunology)</term><term>Death</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Lung (immunology)</term><term>Lung (pathology)</term><term>Membrane Glycoproteins (immunology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Respiratory Distress Syndrome, Adult (genetics)</term><term>Respiratory Distress Syndrome, Adult (immunology)</term><term>Respiratory Distress Syndrome, Adult (mortality)</term><term>Respiratory Distress Syndrome, Adult (virology)</term><term>SARS Virus (immunology)</term><term>SARS Virus (isolation & purification)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (complications)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Spike Glycoprotein, Coronavirus</term><term>Up-Regulation</term><term>Viral Envelope Proteins (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Respiratory Distress Syndrome, Adult</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aging</term><term>Cytokines</term><term>Lung</term><term>Membrane Glycoproteins</term><term>Respiratory Distress Syndrome, Adult</term><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Respiratory Distress Syndrome, Adult</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Respiratory Distress Syndrome, Adult</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Death</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Spike Glycoprotein, Coronavirus</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19420084</PMID><DateCompleted><Year>2009</Year><Month>07</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>83</Volume><Issue>14</Issue><PubDate><Year>2009</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Early upregulation of acute respiratory distress syndrome-associated cytokines promotes lethal disease in an aged-mouse model of severe acute respiratory syndrome coronavirus infection.</ArticleTitle><Pagination><MedlinePgn>7062-74</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00127-09</ELocationID><Abstract><AbstractText>Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rockx</LastName><ForeName>Barry</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of North Carolina, Chapel Hill, North Carolina, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baas</LastName><ForeName>Tracey</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Zornetzer</LastName><ForeName>Gregory A</ForeName><Initials>GA</Initials></Author><Author ValidYN="Y"><LastName>Haagmans</LastName><ForeName>Bart</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Sheahan</LastName><ForeName>Timothy</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Frieman</LastName><ForeName>Matthew</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Dyer</LastName><ForeName>Matthew D</ForeName><Initials>MD</Initials></Author><Author ValidYN="Y"><LastName>Teal</LastName><ForeName>Thomas H</ForeName><Initials>TH</Initials></Author><Author ValidYN="Y"><LastName>Proll</LastName><ForeName>Sean</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>van den Brand</LastName><ForeName>Judith</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Baric</LastName><ForeName>Ralph</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 AI059443</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL080621</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-HL080621</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01-AI059443</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI059136</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI059136</GrantID><Acronym>AI</Acronym><Agency>NIAID 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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>05</Month><Day>06</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="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064370">Spike Glycoprotein, Coronavirus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014759">Viral Envelope Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>J Virol. 2009 Sep;83(17):9022</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003643" MajorTopicYN="N">Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</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="D008562" MajorTopicYN="N">Membrane Glycoproteins</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012128" MajorTopicYN="N">Respiratory Distress Syndrome, Adult</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000401" MajorTopicYN="Y">mortality</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D064370" MajorTopicYN="N">Spike Glycoprotein, Coronavirus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="Y">Up-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014759" MajorTopicYN="N">Viral Envelope 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