Genetic deficiency and polymorphisms of cyclophilin A reveal its essential role for Human Coronavirus 229E replication.
Identifieur interne : 001542 ( PubMed/Checkpoint ); précédent : 001541; suivant : 001543Genetic deficiency and polymorphisms of cyclophilin A reveal its essential role for Human Coronavirus 229E replication.
Auteurs : Albrecht Von Brunn [Allemagne] ; Sandra Ciesek [Allemagne] ; Brigitte Von Brunn [Allemagne] ; Javier Carbajo-Lozoya [Allemagne]Source :
- Current opinion in virology [ 1879-6265 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- déficit : Cyclophiline A.
- génétique : Cyclophiline A.
- métabolisme : Cyclophiline A.
- physiologie : Coronavirus humain 229E.
- Humains, Interactions hôte-pathogène, Polymorphisme de nucléotide simple, Réplication virale.
English descriptors
- KwdEn :
- MESH :
- chemical , deficiency : Cyclophilin A.
- chemical , genetics : Cyclophilin A.
- chemical , metabolism : Cyclophilin A.
- physiology : Coronavirus 229E, Human.
- Host-Pathogen Interactions, Humans, Polymorphism, Single Nucleotide, Virus Replication.
Abstract
Replication of coronaviruses is inhibited in vitro by cyclosporin A, a well-known immunosuppressive drug which binds to cellular cyclophilins thus inactivating their enzymatic cis-trans peptidyl-prolyl isomerase function. Latter is required for proper folding of cellular proteins and of proteins of several viruses. Here, we summarize present knowledge on the role of cyclophilin A during coronavirus replication. We present data on the effect of cyclophilin A single nucleotide polymorphism mutants on the replication of human CoV-229E demonstrating the requirement of proper cyclophilin A function for virus propagation. Results define cellular cyclophilin A as a host target for inhibition of coronaviruses ranging from relatively mild common cold to highly pathogenic SARS-CoV and MERS-CoV viruses with the perspective of disclosing non-immunosuppressive cyclosporin A analogs to broadly inactivate the coronavirus family.
DOI: 10.1016/j.coviro.2015.08.004
PubMed: 26318518
Affiliations:
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Latter is required for proper folding of cellular proteins and of proteins of several viruses. Here, we summarize present knowledge on the role of cyclophilin A during coronavirus replication. We present data on the effect of cyclophilin A single nucleotide polymorphism mutants on the replication of human CoV-229E demonstrating the requirement of proper cyclophilin A function for virus propagation. Results define cellular cyclophilin A as a host target for inhibition of coronaviruses ranging from relatively mild common cold to highly pathogenic SARS-CoV and MERS-CoV viruses with the perspective of disclosing non-immunosuppressive cyclosporin A analogs to broadly inactivate the coronavirus family. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26318518</PMID><DateCompleted><Year>2016</Year><Month>08</Month><Day>02</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-6265</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Current opinion in virology</Title><ISOAbbreviation>Curr Opin Virol</ISOAbbreviation></Journal><ArticleTitle>Genetic deficiency and polymorphisms of cyclophilin A reveal its essential role for Human Coronavirus 229E replication.</ArticleTitle><Pagination><MedlinePgn>56-61</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.coviro.2015.08.004</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1879-6257(15)00114-5</ELocationID><Abstract><AbstractText>Replication of coronaviruses is inhibited in vitro by cyclosporin A, a well-known immunosuppressive drug which binds to cellular cyclophilins thus inactivating their enzymatic cis-trans peptidyl-prolyl isomerase function. Latter is required for proper folding of cellular proteins and of proteins of several viruses. Here, we summarize present knowledge on the role of cyclophilin A during coronavirus replication. We present data on the effect of cyclophilin A single nucleotide polymorphism mutants on the replication of human CoV-229E demonstrating the requirement of proper cyclophilin A function for virus propagation. Results define cellular cyclophilin A as a host target for inhibition of coronaviruses ranging from relatively mild common cold to highly pathogenic SARS-CoV and MERS-CoV viruses with the perspective of disclosing non-immunosuppressive cyclosporin A analogs to broadly inactivate the coronavirus family. </AbstractText><CopyrightInformation>Copyright © 2015 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>von Brunn</LastName><ForeName>Albrecht</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Max-von-Pettenkofer Institute, Ludwig-Maximilians-Universität, München, Germany; German Center for Infection Research (DZIF), Germany. Electronic address: vonbrunn@mvp.uni-muenchen.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ciesek</LastName><ForeName>Sandra</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>German Center for Infection Research (DZIF), Germany; Department of Gastroenterology, Hepatology und Endocrinology, Medizinische Hochschule Hannover, Hannover, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>von Brunn</LastName><ForeName>Brigitte</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Max-von-Pettenkofer Institute, Ludwig-Maximilians-Universität, München, Germany; German Center for Infection Research (DZIF), Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carbajo-Lozoya</LastName><ForeName>Javier</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Max-von-Pettenkofer Institute, Ludwig-Maximilians-Universität, München, Germany; German Center for Infection Research (DZIF), Germany.</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><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>08</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Curr Opin Virol</MedlineTA><NlmUniqueID>101560941</NlmUniqueID><ISSNLinking>1879-6257</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 5.2.1.-</RegistryNumber><NameOfSubstance UI="D021984">Cyclophilin A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D028941" MajorTopicYN="N">Coronavirus 229E, Human</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D021984" MajorTopicYN="N">Cyclophilin A</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="Y">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>07</Month><Day>21</Day></PubMedPubDate><PubMedPubDate 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IdType="pubmed">15928679</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Basse-Saxe</li></region><settlement><li>Hanovre</li></settlement></list><tree><country name="Allemagne"><noRegion><name sortKey="Von Brunn, Albrecht" sort="Von Brunn, Albrecht" uniqKey="Von Brunn A" first="Albrecht" last="Von Brunn">Albrecht Von Brunn</name></noRegion><name sortKey="Carbajo Lozoya, Javier" sort="Carbajo Lozoya, Javier" uniqKey="Carbajo Lozoya J" first="Javier" last="Carbajo-Lozoya">Javier Carbajo-Lozoya</name><name sortKey="Ciesek, Sandra" sort="Ciesek, Sandra" uniqKey="Ciesek S" first="Sandra" last="Ciesek">Sandra Ciesek</name><name sortKey="Von Brunn, Brigitte" sort="Von Brunn, Brigitte" uniqKey="Von Brunn B" first="Brigitte" last="Von Brunn">Brigitte Von Brunn</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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