A new mouse-adapted strain of SARS-CoV as a lethal model for evaluating antiviral agents in vitro and in vivo
Identifieur interne : 002B96 ( Main/Exploration ); précédent : 002B95; suivant : 002B97A new mouse-adapted strain of SARS-CoV as a lethal model for evaluating antiviral agents in vitro and in vivo
Auteurs : Craig W. Day [États-Unis] ; Ralph Baric [États-Unis] ; Sui Xiong Cai [États-Unis] ; Matt Frieman [États-Unis] ; Yohichi Kumaki [États-Unis] ; John D. Morrey [États-Unis] ; Donald F. Smee [États-Unis] ; Dale L. Barnard [États-Unis]Source :
- Virology [ 0042-6822 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Antiviraux (pharmacologie), Cytokines (métabolisme), Femelle, Génome viral, Mutation, Poumon (anatomopathologie), Poumon (métabolisme), Protéines virales (génétique), Protéines virales (métabolisme), Régulation de l'expression des gènes (physiologie), Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (traitement médicamenteux), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (physiologie).
- MESH :
- anatomopathologie : Poumon.
- génétique : Protéines virales.
- métabolisme : Cytokines, Poumon, Protéines virales, Syndrome respiratoire aigu sévère.
- pharmacologie : Antiviraux.
- physiologie : Régulation de l'expression des gènes, Virus du SRAS.
- traitement médicamenteux : Syndrome respiratoire aigu sévère.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Femelle, Génome viral, Mutation, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (pharmacology), Cytokines (metabolism), Female, Gene Expression Regulation (physiology), Genome, Viral, Lung (metabolism), Lung (pathology), Mice, Mice, Inbred BALB C, Mutation, SARS Virus (physiology), Severe Acute Respiratory Syndrome (drug therapy), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Viral Proteins (genetics), Viral Proteins (metabolism).
- MESH :
- chemical , genetics : Viral Proteins.
- chemical , metabolism : Cytokines, Viral Proteins.
- chemical , pharmacology : Antiviral Agents.
- drug therapy : Severe Acute Respiratory Syndrome.
- metabolism : Lung, Severe Acute Respiratory Syndrome.
- pathology : Lung.
- physiology : Gene Expression Regulation, SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Female, Genome, Viral, Mice, Mice, Inbred BALB C, Mutation.
Abstract
Severe acute respiratory syndrome (SARS) is a highly lethal emerging disease caused by coronavirus SARS-CoV. New lethal animal models for SARS were needed to facilitate antiviral research. We adapted and characterized a new strain of SARS-CoV (strain v2163) that was highly lethal in 5- to 6-week-old BALB/c mice. It had nine mutations affecting 10 amino acid residues. Strain v2163 increased IL-1α, IL-6, MIP-1α, MCP-1, and RANTES in mice, and high IL-6 expression correlated with mortality. The infection largely mimicked human disease, but lung pathology lacked hyaline membrane formation. In vitro efficacy against v2163 was shown with known inhibitors of SARS-CoV replication. In v2163-infected mice, Ampligen™ was fully protective, stinging nettle lectin (UDA) was partially protective, ribavirin was disputable and possibly exacerbated disease, and EP128533 was inactive. Ribavirin, UDA, and Ampligen™ decreased IL-6 expression. Strain v2163 provided a valuable model for anti-SARS research.
Url:
DOI: 10.1016/j.virol.2009.09.023
PubMed: 19853271
PubMed Central: 2787736
Affiliations:
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Le document en format XML
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<term>Antiviral Agents (pharmacology)</term>
<term>Cytokines (metabolism)</term>
<term>Female</term>
<term>Gene Expression Regulation (physiology)</term>
<term>Genome, Viral</term>
<term>Lung (metabolism)</term>
<term>Lung (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mutation</term>
<term>SARS Virus (physiology)</term>
<term>Severe Acute Respiratory Syndrome (drug therapy)</term>
<term>Severe Acute Respiratory Syndrome (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Viral Proteins (genetics)</term>
<term>Viral Proteins (metabolism)</term>
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<term>Antiviraux (pharmacologie)</term>
<term>Cytokines (métabolisme)</term>
<term>Femelle</term>
<term>Génome viral</term>
<term>Mutation</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (métabolisme)</term>
<term>Protéines virales (génétique)</term>
<term>Protéines virales (métabolisme)</term>
<term>Régulation de l'expression des gènes (physiologie)</term>
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<term>Souris de lignée BALB C</term>
<term>Syndrome respiratoire aigu sévère (métabolisme)</term>
<term>Syndrome respiratoire aigu sévère (traitement médicamenteux)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virus du SRAS (physiologie)</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>Poumon</term>
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<term>Virus du SRAS</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation</term>
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<front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS) is a highly lethal emerging disease caused by coronavirus SARS-CoV. New lethal animal models for SARS were needed to facilitate antiviral research. We adapted and characterized a new strain of SARS-CoV (strain v2163) that was highly lethal in 5- to 6-week-old BALB/c mice. It had nine mutations affecting 10 amino acid residues. Strain v2163 increased IL-1α, IL-6, MIP-1α, MCP-1, and RANTES in mice, and high IL-6 expression correlated with mortality. The infection largely mimicked human disease, but lung pathology lacked hyaline membrane formation. In vitro efficacy against v2163 was shown with known inhibitors of SARS-CoV replication. In v2163-infected mice, Ampligen™ was fully protective, stinging nettle lectin (UDA) was partially protective, ribavirin was disputable and possibly exacerbated disease, and EP128533 was inactive. Ribavirin, UDA, and Ampligen™ decreased IL-6 expression. Strain v2163 provided a valuable model for anti-SARS research.</p>
</div>
</front>
<back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Balzarini, J" uniqKey="Balzarini J">J. Balzarini</name>
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<biblStruct><analytic><author><name sortKey="Barnard, D L" uniqKey="Barnard D">D.L. Barnard</name>
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<author><name sortKey="Day, C W" uniqKey="Day C">C.W. Day</name>
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<biblStruct><analytic><author><name sortKey="Barnard, D L" uniqKey="Barnard D">D.L. Barnard</name>
</author>
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<author><name sortKey="Carson, D A" uniqKey="Carson D">D.A. Carson</name>
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</div1>
</back>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Caroline du Nord</li>
<li>Utah</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Utah"><name sortKey="Day, Craig W" sort="Day, Craig W" uniqKey="Day C" first="Craig W." last="Day">Craig W. Day</name>
</region>
<name sortKey="Baric, Ralph" sort="Baric, Ralph" uniqKey="Baric R" first="Ralph" last="Baric">Ralph Baric</name>
<name sortKey="Barnard, Dale L" sort="Barnard, Dale L" uniqKey="Barnard D" first="Dale L." last="Barnard">Dale L. Barnard</name>
<name sortKey="Cai, Sui Xiong" sort="Cai, Sui Xiong" uniqKey="Cai S" first="Sui Xiong" last="Cai">Sui Xiong Cai</name>
<name sortKey="Frieman, Matt" sort="Frieman, Matt" uniqKey="Frieman M" first="Matt" last="Frieman">Matt Frieman</name>
<name sortKey="Kumaki, Yohichi" sort="Kumaki, Yohichi" uniqKey="Kumaki Y" first="Yohichi" last="Kumaki">Yohichi Kumaki</name>
<name sortKey="Morrey, John D" sort="Morrey, John D" uniqKey="Morrey J" first="John D." last="Morrey">John D. Morrey</name>
<name sortKey="Smee, Donald F" sort="Smee, Donald F" uniqKey="Smee D" first="Donald F." last="Smee">Donald F. Smee</name>
</country>
</tree>
</affiliations>
</record>
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