SARS-CoV and IFN: Too Little, Too Late.
Identifieur interne : 000F46 ( Main/Exploration ); précédent : 000F45; suivant : 000F47SARS-CoV and IFN: Too Little, Too Late.
Auteurs : Eveline Kindler [Suisse] ; Volker Thiel [Suisse]Source :
- Cell host & microbe [ 1934-6069 ] ; 2016.
Descripteurs français
- KwdFr :
- MESH :
- virologie : Poumon.
- Animaux, Interféron de type I, Réplication virale, Virus du SRAS.
English descriptors
- KwdEn :
- MESH :
- chemical : Interferon Type I.
- virology : Lung.
- Animals, SARS Virus, Virus Replication.
Abstract
Dysregulated type I interferon (IFN-I) expression can lead to severe pathology and disease. In this issue of Cell Host & Microbe, Channappanavar et al. (2016) use a SARS-coronavirus animal model to describe how rapid and robust virus replication with delayed IFN-I can lead to lung immunopathology, with fatal outcomes.
DOI: 10.1016/j.chom.2016.01.012
PubMed: 26867172
Affiliations:
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Le document en format XML
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Electronic address: volker.thiel@vetsuisse.unibe.ch.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Infectious Diseases and Pathobiology, University of Bern, 3012 Bern, Switzerland; Federal Department of Home Affairs, Institute of Virology and Immunology, 3012 Bern and 3147 Mittelhäusern</wicri:regionArea><orgName type="university">Université de Berne</orgName><placeName><settlement type="city">Berne</settlement><region nuts="3" type="region">Canton de Berne</region></placeName></affiliation></author></analytic><series><title level="j">Cell host & microbe</title><idno type="eISSN">1934-6069</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Interferon Type I</term><term>Lung (virology)</term><term>SARS Virus</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Interféron de type I</term><term>Poumon (virologie)</term><term>Réplication virale</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>SARS Virus</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Interféron de type I</term><term>Réplication virale</term><term>Virus du SRAS</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dysregulated type I interferon (IFN-I) expression can lead to severe pathology and disease. In this issue of Cell Host & Microbe, Channappanavar et al. (2016) use a SARS-coronavirus animal model to describe how rapid and robust virus replication with delayed IFN-I can lead to lung immunopathology, with fatal outcomes. </div></front></TEI><affiliations><list><country><li>Suisse</li></country><region><li>Canton de Berne</li></region><settlement><li>Berne</li></settlement><orgName><li>Université de Berne</li></orgName></list><tree><country name="Suisse"><region name="Canton de Berne"><name sortKey="Kindler, Eveline" sort="Kindler, Eveline" uniqKey="Kindler E" first="Eveline" last="Kindler">Eveline Kindler</name></region><name sortKey="Thiel, Volker" sort="Thiel, Volker" uniqKey="Thiel V" first="Volker" last="Thiel">Volker Thiel</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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