Genetic deficiency and polymorphisms of cyclophilin A reveal its essential role for Human Coronavirus 229E replication.
Identifieur interne : 001316 ( Main/Curation ); précédent : 001315; suivant : 001317Genetic 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
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pubmed:26318518Le document en format XML
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<front><div type="abstract" xml:lang="en">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. </div>
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