Genomic Analysis Reveals Age-Dependent Innate Immune Responses to Severe Acute Respiratory Syndrome Coronavirus
Identifieur interne : 000222 ( PascalFrancis/Corpus ); précédent : 000221; suivant : 000223Genomic 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 SubbaraoSource :
- Journal of virology [ 0022-538X ] ; 2008.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Format Inist (serveur)
NO : | PASCAL 09-0185103 INIST |
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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 |
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Pascal:09-0185103Le 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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<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie des poumons</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>138</s1>
</fN21>
</pA>
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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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