HIV protease inhibitor nelfinavir inhibits replication of SARS-associated coronavirus.
Identifieur interne : 002D96 ( PubMed/Curation ); précédent : 002D95; suivant : 002D97HIV protease inhibitor nelfinavir inhibits replication of SARS-associated coronavirus.
Auteurs : Norio Yamamoto [Japon] ; Rongge Yang ; Yoshiyuki Yoshinaka ; Shinji Amari ; Tatsuya Nakano ; Jindrich Cinatl ; Holger Rabenau ; Hans Wilhelm Doerr ; Gerhard Hunsmann ; Akira Otaka ; Hirokazu Tamamura ; Nobutaka Fujii ; Naoki YamamotoSource :
- 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.
DOI: 10.1016/j.bbrc.2004.04.083
PubMed: 15144898
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sort="Yoshinaka, Yoshiyuki" uniqKey="Yoshinaka Y" first="Yoshiyuki" last="Yoshinaka">Yoshiyuki Yoshinaka</name></author><author><name sortKey="Amari, Shinji" sort="Amari, Shinji" uniqKey="Amari S" first="Shinji" last="Amari">Shinji Amari</name></author><author><name sortKey="Nakano, Tatsuya" sort="Nakano, Tatsuya" uniqKey="Nakano T" first="Tatsuya" last="Nakano">Tatsuya Nakano</name></author><author><name sortKey="Cinatl, Jindrich" sort="Cinatl, Jindrich" uniqKey="Cinatl J" first="Jindrich" last="Cinatl">Jindrich Cinatl</name></author><author><name sortKey="Rabenau, Holger" sort="Rabenau, Holger" uniqKey="Rabenau H" first="Holger" last="Rabenau">Holger Rabenau</name></author><author><name sortKey="Doerr, Hans Wilhelm" sort="Doerr, Hans Wilhelm" uniqKey="Doerr H" first="Hans Wilhelm" last="Doerr">Hans Wilhelm Doerr</name></author><author><name sortKey="Hunsmann, Gerhard" sort="Hunsmann, Gerhard" uniqKey="Hunsmann G" first="Gerhard" last="Hunsmann">Gerhard Hunsmann</name></author><author><name sortKey="Otaka, Akira" sort="Otaka, Akira" uniqKey="Otaka A" first="Akira" last="Otaka">Akira Otaka</name></author><author><name sortKey="Tamamura, Hirokazu" sort="Tamamura, Hirokazu" uniqKey="Tamamura H" first="Hirokazu" last="Tamamura">Hirokazu Tamamura</name></author><author><name sortKey="Fujii, Nobutaka" sort="Fujii, Nobutaka" uniqKey="Fujii N" first="Nobutaka" last="Fujii">Nobutaka Fujii</name></author><author><name sortKey="Yamamoto, Naoki" sort="Yamamoto, Naoki" uniqKey="Yamamoto N" first="Naoki" last="Yamamoto">Naoki Yamamoto</name></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="ISSN">0006-291X</idno><imprint><date when="2004" type="published">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">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15144898</PMID><DateCompleted><Year>2004</Year><Month>07</Month><Day>16</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-291X</ISSN><JournalIssue CitedMedium="Print"><Volume>318</Volume><Issue>3</Issue><PubDate><Year>2004</Year><Month>Jun</Month><Day>04</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem. Biophys. Res. Commun.</ISOAbbreviation></Journal><ArticleTitle>HIV protease inhibitor nelfinavir inhibits replication of SARS-associated coronavirus.</ArticleTitle><Pagination><MedlinePgn>719-25</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yamamoto</LastName><ForeName>Norio</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Molecular Virology, Bio-Response, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. yamamoto.mmb@tmd.ac.jp</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Rongge</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Yoshinaka</LastName><ForeName>Yoshiyuki</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Amari</LastName><ForeName>Shinji</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Nakano</LastName><ForeName>Tatsuya</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Cinatl</LastName><ForeName>Jindrich</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Rabenau</LastName><ForeName>Holger</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Doerr</LastName><ForeName>Hans Wilhelm</ForeName><Initials>HW</Initials></Author><Author ValidYN="Y"><LastName>Hunsmann</LastName><ForeName>Gerhard</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Otaka</LastName><ForeName>Akira</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Tamamura</LastName><ForeName>Hirokazu</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Fujii</LastName><ForeName>Nobutaka</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Yamamoto</LastName><ForeName>Naoki</ForeName><Initials>N</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017320">HIV Protease Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012367">RNA, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>HO3OGH5D7I</RegistryNumber><NameOfSubstance UI="D019888">Nelfinavir</NameOfSubstance></Chemical><Chemical><RegistryNumber>O3J8G9O825</RegistryNumber><NameOfSubstance UI="D019438">Ritonavir</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005455" MajorTopicYN="N">Fluorescent Antibody Technique</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017320" MajorTopicYN="N">HIV Protease Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007928" MajorTopicYN="N">Lethal Dose 50</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019888" MajorTopicYN="N">Nelfinavir</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012367" 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