Potent inhibition of SARS-associated coronavirus (SCOV) infection and replication by type I interferons (IFN-alpha/beta) but not by type II interferon (IFN-gamma).
Identifieur interne : 005206 ( Main/Exploration ); précédent : 005205; suivant : 005207Potent inhibition of SARS-associated coronavirus (SCOV) infection and replication by type I interferons (IFN-alpha/beta) but not by type II interferon (IFN-gamma).
Auteurs : Bojian Zheng [Hong Kong] ; Ming-Liang He ; King-Ling Wong ; Ching Tung Lum ; Leo L M. Poon ; Ying Peng ; Yi Guan ; Marie C M. Lin ; Hsiang-Fu KungSource :
- Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research [ 1079-9907 ] ; 2004.
Descripteurs français
- KwdFr :
- ARN viral (biosynthèse), Antiviraux (pharmacologie), Effet cytopathogène viral (), Humains, Interféron de type I (pharmacologie), Interféron gamma (pharmacologie), Lignée cellulaire, RT-PCR, Relation dose-effet des médicaments, Réplication virale (), Transduction du signal (), Virus du SRAS (métabolisme), Virus du SRAS (pathogénicité).
- MESH :
- biosynthèse : ARN viral.
- métabolisme : Virus du SRAS.
- pathogénicité : Virus du SRAS.
- pharmacologie : Antiviraux, Interféron de type I, Interféron gamma.
- Effet cytopathogène viral, Humains, Lignée cellulaire, RT-PCR, Relation dose-effet des médicaments, Réplication virale, Transduction du signal.
English descriptors
- KwdEn :
- Antiviral Agents (pharmacology), Cell Line, Cytopathogenic Effect, Viral (drug effects), Dose-Response Relationship, Drug, Humans, Interferon Type I (pharmacology), Interferon-gamma (pharmacology), RNA, Viral (biosynthesis), Reverse Transcriptase Polymerase Chain Reaction, SARS Virus (metabolism), SARS Virus (pathogenicity), Signal Transduction (drug effects), Virus Replication (drug effects).
- MESH :
- chemical , biosynthesis : RNA, Viral.
- chemical , pharmacology : Antiviral Agents, Interferon Type I, Interferon-gamma.
- drug effects : Cytopathogenic Effect, Viral, Signal Transduction, Virus Replication.
- metabolism : SARS Virus.
- pathogenicity : SARS Virus.
- Cell Line, Dose-Response Relationship, Drug, Humans, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
We sought to investigate the anti-severe acute respiratory syndrome (SARS)-associated coronavirus (SCoV) activities of type I (alpha and beta) and type II (gamma) interferons (IFN) in vitro. Type I IFNs protected cells from cytopathic effects (CPE) induced by SCoV, and inhibited viral genomic RNA replication in FRhk-4 cells (measured by quantitative RT-PCR) in a dose-dependent manner. Intracellular viral RNA copies were reduced 50% by IFN-alpha at a concentration of 25 U/ml and by IFN-beta at a concentration of 14 U/ml. IFN-gamma had fewer effects on inhibition of viral infection and replication. The type I IFN receptor signaling pathway in host cells is mainly involved in the inhibition of SCoV infection and replication. Type I IFNs could be used as potential agents for anti-SARS treatment.
DOI: 10.1089/1079990041535610
PubMed: 15296649
Affiliations:
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Le document en format XML
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Poon</name></author><author><name sortKey="Peng, Ying" sort="Peng, Ying" uniqKey="Peng Y" first="Ying" last="Peng">Ying Peng</name></author><author><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name></author><author><name sortKey="Lin, Marie C M" sort="Lin, Marie C M" uniqKey="Lin M" first="Marie C M" last="Lin">Marie C M. Lin</name></author><author><name sortKey="Kung, Hsiang Fu" sort="Kung, Hsiang Fu" uniqKey="Kung H" first="Hsiang-Fu" last="Kung">Hsiang-Fu Kung</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2004">2004</date><idno type="RBID">pubmed:15296649</idno><idno type="pmid">15296649</idno><idno type="doi">10.1089/1079990041535610</idno><idno type="wicri:Area/PubMed/Corpus">002C33</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002C33</idno><idno type="wicri:Area/PubMed/Curation">002C33</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002C33</idno><idno type="wicri:Area/PubMed/Checkpoint">002B51</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">002B51</idno><idno type="wicri:Area/Ncbi/Merge">000982</idno><idno type="wicri:Area/Ncbi/Curation">000982</idno><idno type="wicri:Area/Ncbi/Checkpoint">000982</idno><idno type="wicri:doubleKey">1079-9907:2004:Zheng B:potent:inhibition:of</idno><idno type="wicri:Area/Main/Merge">005593</idno><idno type="wicri:Area/Main/Curation">005206</idno><idno type="wicri:Area/Main/Exploration">005206</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Potent inhibition of SARS-associated coronavirus (SCOV) infection and replication by type I interferons (IFN-alpha/beta) but not by type II interferon (IFN-gamma).</title><author><name sortKey="Zheng, Bojian" sort="Zheng, Bojian" uniqKey="Zheng B" first="Bojian" last="Zheng">Bojian Zheng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.</nlm:affiliation><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Microbiology, The University of Hong Kong, Pokfulam</wicri:regionArea><wicri:noRegion>Pokfulam</wicri:noRegion></affiliation></author><author><name sortKey="He, Ming Liang" sort="He, Ming Liang" uniqKey="He M" first="Ming-Liang" last="He">Ming-Liang He</name></author><author><name sortKey="Wong, King Ling" sort="Wong, King Ling" uniqKey="Wong K" first="King-Ling" last="Wong">King-Ling Wong</name></author><author><name sortKey="Lum, Ching Tung" sort="Lum, Ching Tung" uniqKey="Lum C" first="Ching Tung" last="Lum">Ching Tung Lum</name></author><author><name sortKey="Poon, Leo L M" sort="Poon, Leo L M" uniqKey="Poon L" first="Leo L M" last="Poon">Leo L M. Poon</name></author><author><name sortKey="Peng, Ying" sort="Peng, Ying" uniqKey="Peng Y" first="Ying" last="Peng">Ying Peng</name></author><author><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name></author><author><name sortKey="Lin, Marie C M" sort="Lin, Marie C M" uniqKey="Lin M" first="Marie C M" last="Lin">Marie C M. Lin</name></author><author><name sortKey="Kung, Hsiang Fu" sort="Kung, Hsiang Fu" uniqKey="Kung H" first="Hsiang-Fu" last="Kung">Hsiang-Fu Kung</name></author></analytic><series><title level="j">Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research</title><idno type="ISSN">1079-9907</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiviral Agents (pharmacology)</term><term>Cell Line</term><term>Cytopathogenic Effect, Viral (drug effects)</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Interferon Type I (pharmacology)</term><term>Interferon-gamma (pharmacology)</term><term>RNA, Viral (biosynthesis)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>SARS Virus (metabolism)</term><term>SARS Virus (pathogenicity)</term><term>Signal Transduction (drug effects)</term><term>Virus Replication (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral (biosynthèse)</term><term>Antiviraux (pharmacologie)</term><term>Effet cytopathogène viral ()</term><term>Humains</term><term>Interféron de type I (pharmacologie)</term><term>Interféron gamma (pharmacologie)</term><term>Lignée cellulaire</term><term>RT-PCR</term><term>Relation dose-effet des médicaments</term><term>Réplication virale ()</term><term>Transduction du signal ()</term><term>Virus du SRAS (métabolisme)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>RNA, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiviral Agents</term><term>Interferon Type I</term><term>Interferon-gamma</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>ARN viral</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cytopathogenic Effect, Viral</term><term>Signal Transduction</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antiviraux</term><term>Interféron de type I</term><term>Interféron gamma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Effet cytopathogène viral</term><term>Humains</term><term>Lignée cellulaire</term><term>RT-PCR</term><term>Relation dose-effet des médicaments</term><term>Réplication virale</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We sought to investigate the anti-severe acute respiratory syndrome (SARS)-associated coronavirus (SCoV) activities of type I (alpha and beta) and type II (gamma) interferons (IFN) in vitro. Type I IFNs protected cells from cytopathic effects (CPE) induced by SCoV, and inhibited viral genomic RNA replication in FRhk-4 cells (measured by quantitative RT-PCR) in a dose-dependent manner. Intracellular viral RNA copies were reduced 50% by IFN-alpha at a concentration of 25 U/ml and by IFN-beta at a concentration of 14 U/ml. IFN-gamma had fewer effects on inhibition of viral infection and replication. The type I IFN receptor signaling pathway in host cells is mainly involved in the inhibition of SCoV infection and replication. Type I IFNs could be used as potential agents for anti-SARS treatment.</div></front></TEI><affiliations><list><country><li>Hong Kong</li></country></list><tree><noCountry><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name><name sortKey="He, Ming Liang" sort="He, Ming Liang" uniqKey="He M" first="Ming-Liang" last="He">Ming-Liang He</name><name sortKey="Kung, Hsiang Fu" sort="Kung, Hsiang Fu" uniqKey="Kung H" first="Hsiang-Fu" last="Kung">Hsiang-Fu Kung</name><name sortKey="Lin, Marie C M" sort="Lin, Marie C M" uniqKey="Lin M" first="Marie C M" last="Lin">Marie C M. Lin</name><name sortKey="Lum, Ching Tung" sort="Lum, Ching Tung" uniqKey="Lum C" first="Ching Tung" last="Lum">Ching Tung Lum</name><name sortKey="Peng, Ying" sort="Peng, Ying" uniqKey="Peng Y" first="Ying" last="Peng">Ying Peng</name><name sortKey="Poon, Leo L M" sort="Poon, Leo L M" uniqKey="Poon L" first="Leo L M" last="Poon">Leo L M. Poon</name><name sortKey="Wong, King Ling" sort="Wong, King Ling" uniqKey="Wong K" first="King-Ling" last="Wong">King-Ling Wong</name></noCountry><country name="Hong Kong"><noRegion><name sortKey="Zheng, Bojian" sort="Zheng, Bojian" uniqKey="Zheng B" first="Bojian" last="Zheng">Bojian Zheng</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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