HIV protease inhibitor nelfinavir inhibits replication of SARS-associated coronavirus
Identifieur interne : 005332 ( Main/Exploration ); précédent : 005331; suivant : 005333HIV protease inhibitor nelfinavir inhibits replication of SARS-associated coronavirus
Auteurs : Norio Yamamoto [Japon] ; Rongge Yang [Japon] ; Yoshiyuki Yoshinaka [Japon] ; Shinji Amari [Japon] ; Tatsuya Nakano [Japon] ; Jindrich Cinatl [Allemagne] ; Holger Rabenau [Allemagne] ; Hans Wilhelm Doerr [Allemagne] ; Gerhard Hunsmann [Allemagne] ; Akira Otaka [Japon] ; Hirokazu Tamamura [Japon] ; Nobutaka Fujii [Japon] ; Naoki Yamamoto [Japon]Source :
- Biochemical and Biophysical Research Communications [ 0006-291X ] ; 2004.
Descripteurs français
- KwdFr :
- ARN viral (analyse), Animaux, Antiviraux (pharmacologie), Cellules Vero, Dose létale 50, Facteurs temps, Inhibiteurs de protéase du VIH (pharmacologie), Nelfinavir (pharmacologie), Ritonavir (pharmacologie), Réplication virale (), Technique d'immunofluorescence, Virus du SRAS (), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- analyse : ARN viral.
- pathogénicité : Virus du SRAS.
- pharmacologie : Antiviraux, Inhibiteurs de protéase du VIH, Nelfinavir, Ritonavir.
- physiologie : Virus du SRAS.
- Animaux, Cellules Vero, Dose létale 50, Facteurs temps, Réplication virale, Technique d'immunofluorescence, Virus du SRAS.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (pharmacology), Chlorocebus aethiops, Fluorescent Antibody Technique, HIV Protease Inhibitors (pharmacology), Lethal Dose 50, Nelfinavir (pharmacology), RNA, Viral (analysis), Ritonavir (pharmacology), SARS Virus (drug effects), SARS Virus (pathogenicity), SARS Virus (physiology), Time Factors, Vero Cells, Virus Replication (drug effects).
- MESH :
- chemical , analysis : RNA, Viral.
- chemical , pharmacology : Antiviral Agents, HIV Protease Inhibitors, Nelfinavir, Ritonavir.
- drug effects : SARS Virus, Virus Replication.
- pathogenicity : SARS Virus.
- physiology : SARS Virus.
- Animals, Chlorocebus aethiops, Fluorescent Antibody Technique, Lethal Dose 50, Time Factors, Vero Cells.
Abstract
A novel coronavirus has been identified as an etiological agent of severe acute respiratory syndrome (SARS). To rapidly identify anti-SARS drugs available for clinical use, we screened a set of compounds that included antiviral drugs already in wide use. Here we report that the HIV-1 protease inhibitor, nelfinavir, strongly inhibited replication of the SARS coronavirus (SARS-CoV). Nelfinavir inhibited the cytopathic effect induced by SARS-CoV infection. Expression of viral antigens was much lower in infected cells treated with nelfinavir than in untreated infected cells. Quantitative RT-PCR analysis showed that nelfinavir could decrease the production of virions from Vero cells. Experiments with various timings of drug addition revealed that nelfinavir exerted its effect not at the entry step, but at the post-entry step of SARS-CoV infection. Our results suggest that nelfinavir should be examined clinically for the treatment of SARS and has potential as a good lead compound for designing anti-SARS drugs.
Url:
DOI: 10.1016/j.bbrc.2004.04.083
PubMed: 15144898
PubMed Central: 7111005
Affiliations:
- Allemagne, Japon
- Basse-Saxe, District de Darmstadt, Hesse (Land), Région de Kantō, Région du Kansai
- Francfort-sur-le-Main, Göttingen, Kyoto, Tokyo
- Université de Kyoto, Université de Tokyo
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Le document en format XML
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<placeName><settlement type="city">Kyoto</settlement>
<region type="prefecture">Région du Kansai</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Yamamoto, Naoki" sort="Yamamoto, Naoki" uniqKey="Yamamoto N" first="Naoki" last="Yamamoto">Naoki Yamamoto</name>
<affiliation wicri:level="1"><nlm:aff id="AFF1">Department of Molecular Virology, Bio-Response, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan</nlm:aff>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Molecular Virology, Bio-Response, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519</wicri:regionArea>
<placeName><settlement type="city">Tokyo</settlement>
<region type="région">Région de Kantō</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Biochemical and Biophysical Research Communications</title>
<idno type="ISSN">0006-291X</idno>
<idno type="eISSN">1090-2104</idno>
<imprint><date when="2004">2004</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Antiviral Agents (pharmacology)</term>
<term>Chlorocebus aethiops</term>
<term>Fluorescent Antibody Technique</term>
<term>HIV Protease Inhibitors (pharmacology)</term>
<term>Lethal Dose 50</term>
<term>Nelfinavir (pharmacology)</term>
<term>RNA, Viral (analysis)</term>
<term>Ritonavir (pharmacology)</term>
<term>SARS Virus (drug effects)</term>
<term>SARS Virus (pathogenicity)</term>
<term>SARS Virus (physiology)</term>
<term>Time Factors</term>
<term>Vero Cells</term>
<term>Virus Replication (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral (analyse)</term>
<term>Animaux</term>
<term>Antiviraux (pharmacologie)</term>
<term>Cellules Vero</term>
<term>Dose létale 50</term>
<term>Facteurs temps</term>
<term>Inhibiteurs de protéase du VIH (pharmacologie)</term>
<term>Nelfinavir (pharmacologie)</term>
<term>Ritonavir (pharmacologie)</term>
<term>Réplication virale ()</term>
<term>Technique d'immunofluorescence</term>
<term>Virus du SRAS ()</term>
<term>Virus du SRAS (pathogénicité)</term>
<term>Virus du SRAS (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>RNA, Viral</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiviral Agents</term>
<term>HIV Protease Inhibitors</term>
<term>Nelfinavir</term>
<term>Ritonavir</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>ARN viral</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>SARS Virus</term>
<term>Virus Replication</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>Inhibiteurs de protéase du VIH</term>
<term>Nelfinavir</term>
<term>Ritonavir</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Chlorocebus aethiops</term>
<term>Fluorescent Antibody Technique</term>
<term>Lethal Dose 50</term>
<term>Time Factors</term>
<term>Vero Cells</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules Vero</term>
<term>Dose létale 50</term>
<term>Facteurs temps</term>
<term>Réplication virale</term>
<term>Technique d'immunofluorescence</term>
<term>Virus du SRAS</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>A novel coronavirus has been identified as an etiological agent of severe acute respiratory syndrome (SARS). To rapidly identify anti-SARS drugs available for clinical use, we screened a set of compounds that included antiviral drugs already in wide use. Here we report that the HIV-1 protease inhibitor, nelfinavir, strongly inhibited replication of the SARS coronavirus (SARS-CoV). Nelfinavir inhibited the cytopathic effect induced by SARS-CoV infection. Expression of viral antigens was much lower in infected cells treated with nelfinavir than in untreated infected cells. Quantitative RT-PCR analysis showed that nelfinavir could decrease the production of virions from Vero cells. Experiments with various timings of drug addition revealed that nelfinavir exerted its effect not at the entry step, but at the post-entry step of SARS-CoV infection. Our results suggest that nelfinavir should be examined clinically for the treatment of SARS and has potential as a good lead compound for designing anti-SARS drugs.</p>
</div>
</front>
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</back>
</TEI>
<affiliations><list><country><li>Allemagne</li>
<li>Japon</li>
</country>
<region><li>Basse-Saxe</li>
<li>District de Darmstadt</li>
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</tree>
</affiliations>
</record>
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