SrasV1, PascalFrancis, Corpus, bibRecord, 000222

Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus

Identifieur interne : 000222 ( PascalFrancis/Corpus ); précédent : 000221; suivant : 000223

Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus

Auteurs : Tracey Baas ; Anjeanette Roberts ; Thomas H. Teal ; Leatrice Vogel ; JUN CHEN ; Terrence M. Tumpey ; Michael G. Katze ; Kanta Subbarao

Source :

Journal of virology [ 0022-538X ] ; 2008.

RBID : Pascal:09-0185103

Descripteurs français

Pascal (Inist)
- Coronavirus, Génomique, Age, Immunité naturelle, Réponse immune, Virologie, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Age, Coronavirus, Genomics, Immune response, Natural immunity, Severe acute respiratory syndrome, Virology.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03		`1`		`@0 J. virol.`
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A11	`02`	`1`		`@1 ROBERTS (Anjeanette)`
A11	`03`	`1`		`@1 TEAL (Thomas H.)`
A11	`04`	`1`		`@1 VOGEL (Leatrice)`
A11	`05`	`1`		`@1 JUN CHEN`
A11	`06`	`1`		`@1 TUMPEY (Terrence M.)`
A11	`07`	`1`		`@1 KATZE (Michael G.)`
A11	`08`	`1`		`@1 SUBBARAO (Kanta)`
A14	`01`			`@1 Department of Microbiology, University of Washington @2 Seattle, Washington @3 USA @Z 1 aut. @Z 3 aut. @Z 7 aut.`
A14	`02`			`@1 Laboratory of Infectious Diseases, NIAID, NIH @2 Bethesda, Maryland @3 USA @Z 2 aut. @Z 4 aut. @Z 5 aut. @Z 8 aut.`
A14	`03`			`@1 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention @2 Atlanta, Georgia @3 USA @Z 6 aut.`
A20				`@1 9465-9476`
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A43	`01`			`@1 INIST @2 13592 @5 354000185759110170`
A44				`@0 0000 @1 © 2009 INIST-CNRS. All rights reserved.`
A45				`@0 43 ref.`
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A64	`01`	`1`		`@0 Journal of virology`
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C01	`01`		`ENG`	@0 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.
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C03	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 01`
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C03	`02`	`X`	`ENG`	`@0 Genomics @5 05`
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C03	`03`	`X`	`FRE`	`@0 Age @5 06`
C03	`03`	`X`	`ENG`	`@0 Age @5 06`
C03	`03`	`X`	`SPA`	`@0 Edad @5 06`
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C03	`05`	`X`	`SPA`	`@0 Respuesta inmune @5 08`
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C03	`07`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 14`
C07	`01`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
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C07	`03`	`X`	`SPA`	`@0 Virus @2 NW`
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C07	`05`	`X`	`FRE`	`@0 Virose`
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C07	`07`	`X`	`ENG`	`@0 Lung disease @5 16`
C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 16`
N21				`@1 138`

Format Inist (serveur)

NO :	PASCAL 09-0185103 INIST
ET :	Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus
AU :	BAAS (Tracey); ROBERTS (Anjeanette); TEAL (Thomas H.); VOGEL (Leatrice); JUN CHEN; TUMPEY (Terrence M.); KATZE (Michael G.); SUBBARAO (Kanta)
AF :	Department of Microbiology, University of Washington/Seattle, Washington/Etats-Unis (1 aut., 3 aut., 7 aut.); Laboratory of Infectious Diseases, NIAID, NIH/Bethesda, Maryland/Etats-Unis (2 aut., 4 aut., 5 aut., 8 aut.); Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention/Atlanta, Georgia/Etats-Unis (6 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2008; Vol. 82; No. 19; Pp. 9465-9476; Bibl. 43 ref.
LA :	Anglais
EA :	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.
CC :	002A05C04
FD :	Coronavirus; Génomique; Age; Immunité naturelle; Réponse immune; Virologie; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons
ED :	Coronavirus; Genomics; Age; Natural immunity; Immune response; Virology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Coronavirus; Genómica; Edad; Inmunidad natural; Respuesta inmune; Virología; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000185759110170
ID :	09-0185103

Links to Exploration step

Pascal:09-0185103

Le document en format XML

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<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>
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<fA14 i1="01"><s1>Department of Microbiology, University of Washington</s1>
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<fA14 i1="02"><s1>Laboratory of Infectious Diseases, NIAID, NIH</s1>
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<fA14 i1="03"><s1>Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention</s1>
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<server><NO>PASCAL 09-0185103 INIST</NO>
<ET>Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus</ET>
<AU>BAAS (Tracey); ROBERTS (Anjeanette); TEAL (Thomas H.); VOGEL (Leatrice); JUN CHEN; TUMPEY (Terrence M.); KATZE (Michael G.); SUBBARAO (Kanta)</AU>
<AF>Department of Microbiology, University of Washington/Seattle, Washington/Etats-Unis (1 aut., 3 aut., 7 aut.); Laboratory of Infectious Diseases, NIAID, NIH/Bethesda, Maryland/Etats-Unis (2 aut., 4 aut., 5 aut., 8 aut.); Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention/Atlanta, Georgia/Etats-Unis (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2008; Vol. 82; No. 19; Pp. 9465-9476; Bibl. 43 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A05C04</CC>
<FD>Coronavirus; Génomique; Age; Immunité naturelle; Réponse immune; Virologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons</FG>
<ED>Coronavirus; Genomics; Age; Natural immunity; Immune response; Virology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Genómica; Edad; Inmunidad natural; Respuesta inmune; Virología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000185759110170</LO>
<ID>09-0185103</ID>
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Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus

Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus

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