MersV1, PubMed, Checkpoint, bibRecord, 000999

Broad-spectrum antiviral activity of the eIF4A inhibitor silvestrol against corona- and picornaviruses.

Identifieur interne : 000999 ( PubMed/Checkpoint ); précédent : 000998; suivant : 000A00

Broad-spectrum antiviral activity of the eIF4A inhibitor silvestrol against corona- and picornaviruses.

Auteurs : Christin Müller [Allemagne] ; Falk W. Schulte [Allemagne] ; Kerstin Lange-Grünweller [Allemagne] ; Wiebke Obermann [Allemagne] ; Ramakanth Madhugiri [Allemagne] ; Stephan Pleschka [Allemagne] ; John Ziebuhr [Allemagne] ; Roland K. Hartmann [Allemagne] ; Arnold Grünweller [Allemagne]

Source :

Antiviral research [ 1872-9096 ] ; 2018.

RBID : pubmed:29258862

Descripteurs français

KwdFr :
- Animaux, Antiviraux (pharmacologie), Cellules Vero, Expression des gènes, Facteurs de transcription (antagonistes et inhibiteurs), Gènes rapporteurs, Humains, Lignée cellulaire, Picornaviridae (), Protéines de liaison à l'ADN (antagonistes et inhibiteurs), Relation dose-effet des médicaments, Régulation de l'expression des gènes viraux (), Triterpènes (pharmacologie).
MESH :
- antagonistes et inhibiteurs : Facteurs de transcription, Protéines de liaison à l'ADN.
- pharmacologie : Antiviraux, Triterpènes.
- Animaux, Cellules Vero, Expression des gènes, Gènes rapporteurs, Humains, Lignée cellulaire, Picornaviridae, Relation dose-effet des médicaments, Régulation de l'expression des gènes viraux.

English descriptors

KwdEn :
- Animals, Antiviral Agents (pharmacology), Cell Line, Chlorocebus aethiops, DNA-Binding Proteins (antagonists & inhibitors), Dose-Response Relationship, Drug, Gene Expression, Gene Expression Regulation, Viral (drug effects), Genes, Reporter, Humans, Picornaviridae (drug effects), Transcription Factors (antagonists & inhibitors), Triterpenes (pharmacology), Vero Cells.
MESH :
- chemical , antagonists & inhibitors : DNA-Binding Proteins, Transcription Factors.
- chemical , pharmacology : Antiviral Agents, Triterpenes.
- drug effects : Gene Expression Regulation, Viral, Picornaviridae.
- Animals, Cell Line, Chlorocebus aethiops, Dose-Response Relationship, Drug, Gene Expression, Genes, Reporter, Humans, Vero Cells.

Abstract

Coronaviruses (CoV) and picornaviruses are plus-strand RNA viruses that use 5' cap-dependent and cap-independent strategies, respectively, for viral mRNA translation initiation. Here, we analyzed the effects of the plant compound silvestrol, a specific inhibitor of the DEAD-box RNA helicase eIF4A, on viral translation using a dual luciferase assay and virus-infected primary cells. Silvestrol was recently shown to have potent antiviral activity in Ebola virus-infected human macrophages. We found that silvestrol is also a potent inhibitor of cap-dependent viral mRNA translation in CoV-infected human embryonic lung fibroblast (MRC-5) cells. EC₅₀ values of 1.3 nM and 3 nM silvestrol were determined for MERS-CoV and HCoV-229E, respectively. For the highly pathogenic MERS-CoV, the potent antiviral activities of silvestrol were also confirmed using peripheral blood mononuclear cells (PBMCs) as a second type of human primary cells. Silvestrol strongly inhibits the expression of CoV structural and nonstructural proteins (N, nsp8) and the formation of viral replication/transcription complexes. Furthermore, potential antiviral effects against human rhinovirus (HRV) A1 and poliovirus type 1 (PV), representing different species in the genus Enterovirus (family Picornaviridae), were investigated. The two viruses employ an internal ribosomal entry site (IRES)-mediated translation initiation mechanism. For PV, which is known to require the activity of eIF4A, an EC₅₀ value of 20 nM silvestrol was determined in MRC-5 cells. The higher EC₅₀ value of 100 nM measured for HRV A1 indicates a less critical role of eIF4A activity in HRV A1 IRES-mediated translation initiation. Taken together, the data reveal a broad-spectrum antiviral activity of silvestrol in infected primary cells by inhibiting eIF4A-dependent viral mRNA translation.

DOI: 10.1016/j.antiviral.2017.12.010
PubMed: 29258862

Affiliations:

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Le document en format XML

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<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>DNA-Binding Proteins (antagonists & inhibitors)</term>
<term>Dose-Response Relationship, Drug</term>
<term>Gene Expression</term>
<term>Gene Expression Regulation, Viral (drug effects)</term>
<term>Genes, Reporter</term>
<term>Humans</term>
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<term>Facteurs de transcription (antagonistes et inhibiteurs)</term>
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<term>Relation dose-effet des médicaments</term>
<term>Régulation de l'expression des gènes viraux ()</term>
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<term>Lignée cellulaire</term>
<term>Picornaviridae</term>
<term>Relation dose-effet des médicaments</term>
<term>Régulation de l'expression des gènes viraux</term>
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<front><div type="abstract" xml:lang="en">Coronaviruses (CoV) and picornaviruses are plus-strand RNA viruses that use 5' cap-dependent and cap-independent strategies, respectively, for viral mRNA translation initiation. Here, we analyzed the effects of the plant compound silvestrol, a specific inhibitor of the DEAD-box RNA helicase eIF4A, on viral translation using a dual luciferase assay and virus-infected primary cells. Silvestrol was recently shown to have potent antiviral activity in Ebola virus-infected human macrophages. We found that silvestrol is also a potent inhibitor of cap-dependent viral mRNA translation in CoV-infected human embryonic lung fibroblast (MRC-5) cells. EC<sub>50</sub>
 values of 1.3 nM and 3 nM silvestrol were determined for MERS-CoV and HCoV-229E, respectively. For the highly pathogenic MERS-CoV, the potent antiviral activities of silvestrol were also confirmed using peripheral blood mononuclear cells (PBMCs) as a second type of human primary cells. Silvestrol strongly inhibits the expression of CoV structural and nonstructural proteins (N, nsp8) and the formation of viral replication/transcription complexes. Furthermore, potential antiviral effects against human rhinovirus (HRV) A1 and poliovirus type 1 (PV), representing different species in the genus Enterovirus (family Picornaviridae), were investigated. The two viruses employ an internal ribosomal entry site (IRES)-mediated translation initiation mechanism. For PV, which is known to require the activity of eIF4A, an EC<sub>50</sub>
 value of 20 nM silvestrol was determined in MRC-5 cells. The higher EC<sub>50</sub>
 value of 100 nM measured for HRV A1 indicates a less critical role of eIF4A activity in HRV A1 IRES-mediated translation initiation. Taken together, the data reveal a broad-spectrum antiviral activity of silvestrol in infected primary cells by inhibiting eIF4A-dependent viral mRNA translation.</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>06</Month>
<Day>21</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>04</Month>
<Day>07</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-9096</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>150</Volume>
<PubDate><Year>2018</Year>
<Month>02</Month>
</PubDate>
</JournalIssue>
<Title>Antiviral research</Title>
<ISOAbbreviation>Antiviral Res.</ISOAbbreviation>
</Journal>
<ArticleTitle>Broad-spectrum antiviral activity of the eIF4A inhibitor silvestrol against corona- and picornaviruses.</ArticleTitle>
<Pagination><MedlinePgn>123-129</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0166-3542(17)30638-1</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.antiviral.2017.12.010</ELocationID>
<Abstract><AbstractText>Coronaviruses (CoV) and picornaviruses are plus-strand RNA viruses that use 5' cap-dependent and cap-independent strategies, respectively, for viral mRNA translation initiation. Here, we analyzed the effects of the plant compound silvestrol, a specific inhibitor of the DEAD-box RNA helicase eIF4A, on viral translation using a dual luciferase assay and virus-infected primary cells. Silvestrol was recently shown to have potent antiviral activity in Ebola virus-infected human macrophages. We found that silvestrol is also a potent inhibitor of cap-dependent viral mRNA translation in CoV-infected human embryonic lung fibroblast (MRC-5) cells. EC<sub>50</sub>
 values of 1.3 nM and 3 nM silvestrol were determined for MERS-CoV and HCoV-229E, respectively. For the highly pathogenic MERS-CoV, the potent antiviral activities of silvestrol were also confirmed using peripheral blood mononuclear cells (PBMCs) as a second type of human primary cells. Silvestrol strongly inhibits the expression of CoV structural and nonstructural proteins (N, nsp8) and the formation of viral replication/transcription complexes. Furthermore, potential antiviral effects against human rhinovirus (HRV) A1 and poliovirus type 1 (PV), representing different species in the genus Enterovirus (family Picornaviridae), were investigated. The two viruses employ an internal ribosomal entry site (IRES)-mediated translation initiation mechanism. For PV, which is known to require the activity of eIF4A, an EC<sub>50</sub>
 value of 20 nM silvestrol was determined in MRC-5 cells. The higher EC<sub>50</sub>
 value of 100 nM measured for HRV A1 indicates a less critical role of eIF4A activity in HRV A1 IRES-mediated translation initiation. Taken together, the data reveal a broad-spectrum antiviral activity of silvestrol in infected primary cells by inhibiting eIF4A-dependent viral mRNA translation.</AbstractText>
<CopyrightInformation>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Müller</LastName>
<ForeName>Christin</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Institut für Medizinische Virologie, Justus-Liebig-Universität Gießen, Schubertstraße 81, 35392 Gießen, Germany; Deutsches Zentrum für Infektionsforschung (DZIF) at the partner site Gießen-Marburg-Langen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schulte</LastName>
<ForeName>Falk W</ForeName>
<Initials>FW</Initials>
<AffiliationInfo><Affiliation>Institut für Pharmazeutische Chemie, Philipps-Universität Marburg, Marbacher Weg 6, 35037 Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lange-Grünweller</LastName>
<ForeName>Kerstin</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Institut für Pharmazeutische Chemie, Philipps-Universität Marburg, Marbacher Weg 6, 35037 Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Obermann</LastName>
<ForeName>Wiebke</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Institut für Pharmazeutische Chemie, Philipps-Universität Marburg, Marbacher Weg 6, 35037 Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Madhugiri</LastName>
<ForeName>Ramakanth</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Institut für Medizinische Virologie, Justus-Liebig-Universität Gießen, Schubertstraße 81, 35392 Gießen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pleschka</LastName>
<ForeName>Stephan</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Institut für Medizinische Virologie, Justus-Liebig-Universität Gießen, Schubertstraße 81, 35392 Gießen, Germany; Deutsches Zentrum für Infektionsforschung (DZIF) at the partner site Gießen-Marburg-Langen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ziebuhr</LastName>
<ForeName>John</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Institut für Medizinische Virologie, Justus-Liebig-Universität Gießen, Schubertstraße 81, 35392 Gießen, Germany; Deutsches Zentrum für Infektionsforschung (DZIF) at the partner site Gießen-Marburg-Langen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hartmann</LastName>
<ForeName>Roland K</ForeName>
<Initials>RK</Initials>
<AffiliationInfo><Affiliation>Institut für Pharmazeutische Chemie, Philipps-Universität Marburg, Marbacher Weg 6, 35037 Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Grünweller</LastName>
<ForeName>Arnold</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Institut für Pharmazeutische Chemie, Philipps-Universität Marburg, Marbacher Weg 6, 35037 Marburg, Germany. Electronic address: gruenwel@staff.uni-marburg.de.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>12</Month>
<Day>16</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Antiviral Res</MedlineTA>
<NlmUniqueID>8109699</NlmUniqueID>
<ISSNLinking>0166-3542</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C111931">ELF4 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014315">Triterpenes</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<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="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015967" MajorTopicYN="N">Gene Expression Regulation, Viral</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017930" MajorTopicYN="N">Genes, Reporter</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010849" MajorTopicYN="N">Picornaviridae</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
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<MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D014709" MajorTopicYN="N">Vero Cells</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cap-dependent translation</Keyword>
<Keyword MajorTopicYN="Y">Coronavirus</Keyword>
<Keyword MajorTopicYN="Y">IRES</Keyword>
<Keyword MajorTopicYN="Y">Picornavirus</Keyword>
<Keyword MajorTopicYN="Y">Silvestrol</Keyword>
<Keyword MajorTopicYN="Y">eIF4A</Keyword>
</KeywordList>
</MedlineCitation>
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<Month>12</Month>
<Day>12</Day>
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<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>12</Month>
<Day>14</Day>
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<affiliations><list><country><li>Allemagne</li>
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<tree><country name="Allemagne"><noRegion><name sortKey="Muller, Christin" sort="Muller, Christin" uniqKey="Muller C" first="Christin" last="Müller">Christin Müller</name>
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Broad-spectrum antiviral activity of the eIF4A inhibitor silvestrol against corona- and picornaviruses.

Broad-spectrum antiviral activity of the eIF4A inhibitor silvestrol against corona- and picornaviruses.

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