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Genetic deficiency and polymorphisms of cyclophilin A reveal its essential role for Human Coronavirus 229E replication.

Identifieur interne : 001316 ( Main/Exploration ); précédent : 001315; suivant : 001317

Genetic 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 :

RBID : pubmed:26318518

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English descriptors

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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