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Induction of interferon-gamma-inducible protein 10 by SARS-CoV infection, interferon alfacon 1 and interferon inducer in human bronchial epithelial Calu-3 cells and BALB/c mice.

Identifieur interne : 002516 ( Main/Exploration ); précédent : 002515; suivant : 002517

Induction of interferon-gamma-inducible protein 10 by SARS-CoV infection, interferon alfacon 1 and interferon inducer in human bronchial epithelial Calu-3 cells and BALB/c mice.

Auteurs : Yohichi Kumaki [États-Unis] ; Craig W. Day ; Kevin W. Bailey ; Miles K. Wandersee ; Min-Hui Wong ; Jason R. Madsen ; Justin S. Madsen ; Nathan M. Nelson ; Justin D. Hoopes ; John D. Woolcott ; Tyler Z. Mclean ; Lawrence M. Blatt ; Andres M. Salazar ; Donald F. Smee ; Dale L. Barnard

Source :

RBID : pubmed:20231782

Descripteurs français

English descriptors

Abstract

The pathogenesis of severe acute respiratory syndrome coronavirus (SARS-CoV) is poorly understood. Several mechanisms involving both direct effects on target cells and indirect effects via the immune system might exist. SARS-CoV has been shown in vitro to induce changes of cytokines and chemokines in various human and animal cells. We previously reported that interferon (IFN) alfacon-1 was more active against SARS-CoV infection in human bronchial epithelial Calu-3 cells than in African green monkey kidney epithelial cells on day 3 post-infection.

DOI: 10.3851/IMP1477
PubMed: 20231782


Affiliations:


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Le document en format XML

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<title level="j">Antiviral chemistry & chemotherapy</title>
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<term>Carboxymethylcellulose Sodium (analogs & derivatives)</term>
<term>Carboxymethylcellulose Sodium (pharmacology)</term>
<term>Chemokine CXCL10 (biosynthesis)</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Epithelial Cells (drug effects)</term>
<term>Epithelial Cells (immunology)</term>
<term>Epithelial Cells (virology)</term>
<term>Female</term>
<term>Humans</term>
<term>Interferon Inducers (pharmacology)</term>
<term>Interferon Type I (pharmacology)</term>
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<term>Lung (immunology)</term>
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<term>Severe Acute Respiratory Syndrome (immunology)</term>
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<term>Carboxyméthylcellulose de sodium (pharmacologie)</term>
<term>Cellules épithéliales ()</term>
<term>Cellules épithéliales (immunologie)</term>
<term>Cellules épithéliales (virologie)</term>
<term>Chimiokine CXCL10 (biosynthèse)</term>
<term>Femelle</term>
<term>Humains</term>
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<term>Interféron de type I (pharmacologie)</term>
<term>Organismes exempts d'organismes pathogènes spécifiques</term>
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<term>Polylysine (analogues et dérivés)</term>
<term>Polylysine (pharmacologie)</term>
<term>Poumon ()</term>
<term>Poumon (immunologie)</term>
<term>Poumon (virologie)</term>
<term>Protéines recombinantes</term>
<term>Réplication virale ()</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (traitement médicamenteux)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Test ELISA</term>
<term>Virus du SRAS (physiologie)</term>
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<term>Chemokine CXCL10</term>
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<term>Interferon Inducers</term>
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<front>
<div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome coronavirus (SARS-CoV) is poorly understood. Several mechanisms involving both direct effects on target cells and indirect effects via the immune system might exist. SARS-CoV has been shown in vitro to induce changes of cytokines and chemokines in various human and animal cells. We previously reported that interferon (IFN) alfacon-1 was more active against SARS-CoV infection in human bronchial epithelial Calu-3 cells than in African green monkey kidney epithelial cells on day 3 post-infection.</div>
</front>
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