Suppression of Coronavirus Replication by Cyclophilin Inhibitors
Identifieur interne : 001924 ( Pmc/Curation ); précédent : 001923; suivant : 001925Suppression of Coronavirus Replication by Cyclophilin Inhibitors
Auteurs : Yoshikazu Tanaka [Japon] ; Yuka Sato [Japon] ; Takashi Sasaki [Japon]Source :
- Viruses [ 1999-4915 ] ; 2013.
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.
Url:
DOI: 10.3390/v5051250
PubMed: 23698397
PubMed Central: 3712306
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<front><div type="abstract" xml:lang="en"><p>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.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Viruses</journal-id>
<journal-id journal-id-type="iso-abbrev">Viruses</journal-id>
<journal-id journal-id-type="publisher-id">viruses</journal-id>
<journal-title-group><journal-title>Viruses</journal-title>
</journal-title-group>
<issn pub-type="epub">1999-4915</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23698397</article-id>
<article-id pub-id-type="pmc">3712306</article-id>
<article-id pub-id-type="doi">10.3390/v5051250</article-id>
<article-id pub-id-type="publisher-id">viruses-05-01250</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Suppression of Coronavirus Replication by Cyclophilin Inhibitors</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Tanaka</surname>
<given-names>Yoshikazu</given-names>
</name>
<xref ref-type="aff" rid="af1-viruses-05-01250">1</xref>
<xref rid="c1-viruses-05-01250" ref-type="corresp">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sato</surname>
<given-names>Yuka</given-names>
</name>
<xref ref-type="aff" rid="af2-viruses-05-01250">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sasaki</surname>
<given-names>Takashi</given-names>
</name>
<xref ref-type="aff" rid="af3-viruses-05-01250">3</xref>
</contrib>
</contrib-group>
<aff id="af1-viruses-05-01250"><label>1</label>
Department of Veterinary Hygiene, Veterinary School, Nippon Veterinary & Life Science University, Tokyo 180-8602, Japan</aff>
<aff id="af2-viruses-05-01250"><label>2</label>
Department of Microbiology and Immunology, Division of Molecular Virology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan</aff>
<aff id="af3-viruses-05-01250"><label>3</label>
Laboratory of Bacterial Genomics, Pathogen Genomics Center, National Institute of Infectious Diseases, Tokyo 162-8640, Japan</aff>
<author-notes><corresp id="c1-viruses-05-01250"><label>*</label>
Author to whom correspondence should be addressed; E-Mail: <email>ytanaka@nvlu.ac.jp</email>
; Tel.: +81-422-31-4151; Fax: +81-422-30-7502.</corresp>
</author-notes>
<pub-date pub-type="epub"><day>22</day>
<month>5</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="collection"><month>5</month>
<year>2013</year>
</pub-date>
<volume>5</volume>
<issue>5</issue>
<fpage>1250</fpage>
<lpage>1260</lpage>
<history><date date-type="received"><day>18</day>
<month>3</month>
<year>2013</year>
</date>
<date date-type="rev-recd"><day>02</day>
<month>5</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>08</day>
<month>5</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>© 2013 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement>
<copyright-year>2013</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/3.0/"><license-p>This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (<uri xlink:type="simple" xlink:href="http://creativecommons.org/licenses/by/3.0/">http://creativecommons.org/licenses/by/3.0/</uri>
).</license-p>
</license>
</permissions>
<abstract><p>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.</p>
</abstract>
<kwd-group><kwd>cyclophilin</kwd>
<kwd>cyclosporin A</kwd>
<kwd>coronavirus</kwd>
<kwd>NF-AT</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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