Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus
Identifieur interne : 003501 ( Main/Exploration ); précédent : 003500; suivant : 003502Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus
Auteurs : Tracey Baas [États-Unis] ; Anjeanette Roberts [États-Unis] ; Thomas H. Teal [États-Unis] ; Leatrice Vogel [États-Unis] ; JUN CHEN [États-Unis] ; Terrence M. Tumpey [États-Unis] ; Michael G. Katze [États-Unis] ; Kanta Subbarao [États-Unis]Source :
- Journal of virology [ 0022-538X ] ; 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.
- Pascal (Inist)
English descriptors
- KwdEn :
- Age, Animals, Coronavirus, Enzyme-Linked Immunosorbent Assay, Genome, Genomics, Immune System (virology), Immune response, Immunity, Innate, Lymphocytes (metabolism), Lymphocytes (virology), Mice, Mice, Inbred BALB C, Models, Biological, Natural immunity, Oligonucleotide Array Sequence Analysis, RNA, Messenger (metabolism), SARS Virus (genetics), SARS Virus (metabolism), Severe acute respiratory syndrome, Time Factors, Virology, 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, II6, 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.
Url:
Affiliations:
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Teal</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Microbiology, University of Washington</s1><s2>Seattle, Washington</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Vogel, Leatrice" sort="Vogel, Leatrice" uniqKey="Vogel L" first="Leatrice" last="Vogel">Leatrice Vogel</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Laboratory of Infectious Diseases, NIAID, NIH</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Jun Chen" sort="Jun Chen" uniqKey="Jun Chen" last="Jun Chen">JUN CHEN</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Laboratory of Infectious Diseases, NIAID, NIH</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Tumpey, Terrence M" sort="Tumpey, Terrence M" uniqKey="Tumpey T" first="Terrence M." last="Tumpey">Terrence M. Tumpey</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention</s1><s2>Atlanta, Georgia</s2><s3>USA</s3><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G." last="Katze">Michael G. Katze</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Microbiology, University of Washington</s1><s2>Seattle, Washington</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Laboratory of Infectious Diseases, NIAID, NIH</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age</term><term>Animals</term><term>Coronavirus</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Genome</term><term>Genomics</term><term>Immune System (virology)</term><term>Immune response</term><term>Immunity, Innate</term><term>Lymphocytes (metabolism)</term><term>Lymphocytes (virology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Models, Biological</term><term>Natural immunity</term><term>Oligonucleotide Array Sequence Analysis</term><term>RNA, Messenger (metabolism)</term><term>SARS Virus (genetics)</term><term>SARS Virus (metabolism)</term><term>Severe acute respiratory syndrome</term><term>Time Factors</term><term>Virology</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Animaux</term><term>Facteurs temps</term><term>Génome</term><term>Génomique</term><term>Immunité innée</term><term>Lymphocytes (métabolisme)</term><term>Lymphocytes (virologie)</term><term>Modèles biologiques</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Système immunitaire (virologie)</term><term>Séquençage par oligonucléotides en batterie</term><term>Test ELISA</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lymphocytes</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Lymphocytes</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Lymphocytes</term><term>Système immunitaire</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Immune System</term><term>Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Genome</term><term>Genomics</term><term>Immunity, Innate</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Models, Biological</term><term>Oligonucleotide Array Sequence Analysis</term><term>Time Factors</term><term>Virus Replication</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Animaux</term><term>Coronavirus</term><term>Facteurs temps</term><term>Génome</term><term>Génomique</term><term>Age</term><term>Immunité innée</term><term>Immunité naturelle</term><term>Modèles biologiques</term><term>Réplication virale</term><term>Réponse immune</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Séquençage par oligonucléotides en batterie</term><term>Test ELISA</term><term>Virologie</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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, II6, 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><affiliations><list><country><li>États-Unis</li></country><region><li>Géorgie (États-Unis)</li><li>Maryland</li><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><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><name sortKey="Jun Chen" sort="Jun Chen" uniqKey="Jun Chen" last="Jun Chen">JUN CHEN</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G." last="Katze">Michael G. 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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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