Genomic analysis reveals age-dependent innate immune responses to severe acute respiratory syndrome coronavirus.
Identifieur interne : 001B25 ( PubMed/Checkpoint ); précédent : 001B24; suivant : 001B26Genomic analysis reveals age-dependent innate immune responses to severe acute respiratory syndrome coronavirus.
Auteurs : Tracey Baas [États-Unis] ; Anjeanette Roberts ; Thomas H. Teal ; Leatrice Vogel ; Jun Chen ; Terrence M. Tumpey ; Michael G. Katze ; Kanta SubbaraoSource :
- Journal of virology [ 1098-5514 ] ; 2008.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Animaux, Facteurs temps, Génome, Génomique, Immunité innée, Lymphocytes (métabolisme), Lymphocytes (virologie), Modèles biologiques, Réplication virale, Souris, Souris de lignée BALB C, Système immunitaire (virologie), Séquençage par oligonucléotides en batterie, Test ELISA, Virus du SRAS (génétique), Virus du SRAS (métabolisme).
- MESH :
- génétique : Virus du SRAS.
- métabolisme : ARN messager, Lymphocytes, Virus du SRAS.
- virologie : Lymphocytes, Système immunitaire.
- Animaux, Facteurs temps, Génome, Génomique, Immunité innée, Modèles biologiques, Réplication virale, Souris, Souris de lignée BALB C, Séquençage par oligonucléotides en batterie, Test ELISA.
English descriptors
- KwdEn :
- Animals, Enzyme-Linked Immunosorbent Assay, Genome, Genomics, Immune System (virology), Immunity, Innate, Lymphocytes (metabolism), Lymphocytes (virology), Mice, Mice, Inbred BALB C, Models, Biological, Oligonucleotide Array Sequence Analysis, RNA, Messenger (metabolism), SARS Virus (genetics), SARS Virus (metabolism), Time Factors, Virus Replication.
- MESH :
- chemical , metabolism : RNA, Messenger.
- genetics : SARS Virus.
- metabolism : Lymphocytes, SARS Virus.
- virology : Immune System, Lymphocytes.
- Animals, Enzyme-Linked Immunosorbent Assay, Genome, Genomics, Immunity, Innate, Mice, Mice, Inbred BALB C, Models, Biological, Oligonucleotide Array Sequence Analysis, Time Factors, Virus Replication.
Abstract
The relationship between immunosenescence and the host response to virus infection is poorly understood at the molecular level. Two different patterns of pulmonary host responses to virus were observed when gene expression profiles from severe acute respiratory syndrome coronavirus (SARS-CoV)-infected young mice that show minimal disease were compared to those from SARS-CoV-infected aged mice that develop pneumonitis. In young mice, genes related to cellular development, cell growth, and cell cycle were downregulated during peak viral replication, and these transcripts returned to basal levels as virus was cleared. In contrast, aged mice had a greater number of upregulated immune response and cell-to-cell signaling genes, and the expression of many genes was sustained even after viral clearance, suggesting an exacerbated host response to virus. Interestingly, in SARS-CoV-infected aged mice, a subset of genes, including Tnfa, Il6, Ccl2, Ccl3, Cxcl10, and Ifng, was induced in a biphasic pattern that correlated with peak viral replication and a subsequent influx of lymphocytes and severe histopathologic changes in the lungs. We provide insight into gene expression profiles and molecular signatures underlying immunosenescence in the context of the host response to viral infection.
DOI: 10.1128/JVI.00489-08
PubMed: 18632870
Affiliations:
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Two different patterns of pulmonary host responses to virus were observed when gene expression profiles from severe acute respiratory syndrome coronavirus (SARS-CoV)-infected young mice that show minimal disease were compared to those from SARS-CoV-infected aged mice that develop pneumonitis. In young mice, genes related to cellular development, cell growth, and cell cycle were downregulated during peak viral replication, and these transcripts returned to basal levels as virus was cleared. In contrast, aged mice had a greater number of upregulated immune response and cell-to-cell signaling genes, and the expression of many genes was sustained even after viral clearance, suggesting an exacerbated host response to virus. Interestingly, in SARS-CoV-infected aged mice, a subset of genes, including Tnfa, Il6, Ccl2, Ccl3, Cxcl10, and Ifng, was induced in a biphasic pattern that correlated with peak viral replication and a subsequent influx of lymphocytes and severe histopathologic changes in the lungs. We provide insight into gene expression profiles and molecular signatures underlying immunosenescence in the context of the host response to viral infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18632870</PMID><DateCompleted><Year>2008</Year><Month>10</Month><Day>09</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>82</Volume><Issue>19</Issue><PubDate><Year>2008</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Genomic analysis reveals age-dependent innate immune responses to severe acute respiratory syndrome coronavirus.</ArticleTitle><Pagination><MedlinePgn>9465-76</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00489-08</ELocationID><Abstract><AbstractText>The relationship between immunosenescence and the host response to virus infection is poorly understood at the molecular level. Two different patterns of pulmonary host responses to virus were observed when gene expression profiles from severe acute respiratory syndrome coronavirus (SARS-CoV)-infected young mice that show minimal disease were compared to those from SARS-CoV-infected aged mice that develop pneumonitis. In young mice, genes related to cellular development, cell growth, and cell cycle were downregulated during peak viral replication, and these transcripts returned to basal levels as virus was cleared. In contrast, aged mice had a greater number of upregulated immune response and cell-to-cell signaling genes, and the expression of many genes was sustained even after viral clearance, suggesting an exacerbated host response to virus. Interestingly, in SARS-CoV-infected aged mice, a subset of genes, including Tnfa, Il6, Ccl2, Ccl3, Cxcl10, and Ifng, was induced in a biphasic pattern that correlated with peak viral replication and a subsequent influx of lymphocytes and severe histopathologic changes in the lungs. We provide insight into gene expression profiles and molecular signatures underlying immunosenescence in the context of the host response to viral infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baas</LastName><ForeName>Tracey</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Box 358070, University of Washington, Seattle, WA 98195-8070, USA. traceybaas@gmail.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roberts</LastName><ForeName>Anjeanette</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Teal</LastName><ForeName>Thomas H</ForeName><Initials>TH</Initials></Author><Author ValidYN="Y"><LastName>Vogel</LastName><ForeName>Leatrice</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Jun</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Tumpey</LastName><ForeName>Terrence M</ForeName><Initials>TM</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Subbarao</LastName><ForeName>Kanta</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL080621-01</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P51 RR000166</GrantID><Acronym>RR</Acronym><Agency>NCRR 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><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P51 RR00166-45</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal 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Katze</name><name sortKey="Roberts, Anjeanette" sort="Roberts, Anjeanette" uniqKey="Roberts A" first="Anjeanette" last="Roberts">Anjeanette Roberts</name><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name><name sortKey="Teal, Thomas H" sort="Teal, Thomas H" uniqKey="Teal T" first="Thomas H" last="Teal">Thomas H. Teal</name><name sortKey="Tumpey, Terrence M" sort="Tumpey, Terrence M" uniqKey="Tumpey T" first="Terrence M" last="Tumpey">Terrence M. Tumpey</name><name sortKey="Vogel, Leatrice" sort="Vogel, Leatrice" uniqKey="Vogel L" first="Leatrice" last="Vogel">Leatrice Vogel</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Baas, Tracey" sort="Baas, Tracey" uniqKey="Baas T" first="Tracey" last="Baas">Tracey Baas</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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