Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 May 22;5(5):1250-60.
doi: 10.3390/v5051250.

Suppression of coronavirus replication by cyclophilin inhibitors

Affiliations
Review

Suppression of coronavirus replication by cyclophilin inhibitors

Yoshikazu Tanaka et al. Viruses. .

Abstract

Coronaviruses infect a variety of mammalian and avian species and cause serious diseases in humans, cats, mice, and birds in the form of severe acute respiratory syndrome (SARS), feline infectious peritonitis (FIP), mouse hepatitis, and avian infectious bronchitis, respectively. No effective vaccine or treatment has been developed for SARS-coronavirus or FIP virus, both of which cause lethal diseases. It has been reported that a cyclophilin inhibitor, cyclosporin A (CsA), could inhibit the replication of coronaviruses. CsA is a well-known immunosuppressive drug that binds to cellular cyclophilins to inhibit calcineurin, a calcium-calmodulin-activated serine/threonine-specific phosphatase. The inhibition of calcineurin blocks the translocation of nuclear factor of activated T cells from the cytosol into the nucleus, thus preventing the transcription of genes encoding cytokines such as interleukin-2. Cyclophilins are peptidyl-prolyl isomerases with physiological functions that have been described for many years to include chaperone and foldase activities. Also, many viruses require cyclophilins for replication; these include human immunodeficiency virus, vesicular stomatitis virus, and hepatitis C virus. However, the molecular mechanisms leading to the suppression of viral replication differ for different viruses. This review describes the suppressive effects of CsA on coronavirus replication.

PubMed Disclaimer

Figures

Figure 1
Figure 1
The functions of Cyps in the NF-AT pathway and a hypothesis of the interaction between Cyps and coronavirus. Nsp1 protein enhances NF-AT activities with Ca2+. The activities result in production of IL-2. Although CsA inhibits CoV replication, little is known about the exact role of Cyps in CoV replication.

Similar articles

Cited by

References

    1. Perlman S., Netland J. Coronaviruses post-sars: Update on replication and pathogenesis. Nat. Rev. Microbiol. 2009;7:439–450. doi: 10.1038/nrmicro2147. - DOI - PMC - PubMed
    1. Namy O., Moran S.J., Stuart D.I., Gilbert R.J., Brierley I. A mechanical explanation of RNA pseudoknot function in programmed ribosomal frameshifting. Nature. 2006;441:244–247. doi: 10.1038/nature04735. - DOI - PMC - PubMed
    1. Sawicki S.G., Sawicki D.L., Siddell S.G. A contemporary view of coronavirus transcription. J. Virol. 2007;81:20–29. doi: 10.1128/JVI.01358-06. - DOI - PMC - PubMed
    1. Quesniaux V.F., Schreier M.H., Wenger R.M., Hiestand P.C., Harding M.W., van Regenmortel M.H. Cyclophilin binds to the region of cyclosporine involved in its immunosuppressive activity. Eur. J. Immunol. 1987;17:1359–1365. doi: 10.1002/eji.1830170921. - DOI - PubMed
    1. Wang P., Heitman J. The cyclophilins. Genome Biol. 2005;6:e226. doi: 10.1186/gb-2005-6-7-226. - DOI - PMC - PubMed

Publication types

MeSH terms

-