Suppression of Coronavirus Replication by Cyclophilin Inhibitors
Identifieur interne : 001852 ( Main/Exploration ); précédent : 001851; suivant : 001853Suppression of Coronavirus Replication by Cyclophilin Inhibitors
Auteurs : Yoshikazu Tanaka [Japon] ; Yuka Sato [Japon] ; Takashi Sasaki [Japon]Source :
- Viruses [ 1999-4915 ] ; 2013.
Descripteurs français
- KwdFr :
- MESH :
- antagonistes et inhibiteurs : Cyclophilines.
- métabolisme : Cyclophilines.
- pharmacologie : Antiviraux, Ciclosporine.
- physiologie : Coronavirus.
- Interactions hôte-pathogène, Réplication virale.
English descriptors
- KwdEn :
- MESH :
- chemical , antagonists & inhibitors : Cyclophilins.
- chemical , metabolism : Cyclophilins.
- chemical , pharmacology : Antiviral Agents, Cyclosporine.
- physiology : Coronavirus.
- Host-Pathogen Interactions, Virus Replication.
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
Affiliations:
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Replication by Cyclophilin Inhibitors</title><author><name sortKey="Tanaka, Yoshikazu" sort="Tanaka, Yoshikazu" uniqKey="Tanaka Y" first="Yoshikazu" last="Tanaka">Yoshikazu Tanaka</name><affiliation wicri:level="1"><nlm:aff id="af1-viruses-05-01250">Department of Veterinary Hygiene, Veterinary School, Nippon Veterinary & Life Science University, Tokyo 180-8602, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Veterinary Hygiene, Veterinary School, Nippon Veterinary & Life Science University, Tokyo 180-8602</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Sato, Yuka" sort="Sato, Yuka" uniqKey="Sato Y" first="Yuka" last="Sato">Yuka Sato</name><affiliation wicri:level="4"><nlm:aff id="af2-viruses-05-01250">Department of Microbiology and Immunology, Division of Molecular Virology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology and Immunology, Division of Molecular Virology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName><orgName type="university">Université de Tokyo</orgName><placeName><settlement type="city">Tokyo</settlement><region type="province">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Sasaki, Takashi" sort="Sasaki, Takashi" uniqKey="Sasaki T" first="Takashi" last="Sasaki">Takashi Sasaki</name><affiliation wicri:level="1"><nlm:aff id="af3-viruses-05-01250">Laboratory of Bacterial Genomics, Pathogen Genomics Center, National Institute of Infectious Diseases, Tokyo 162-8640, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Bacterial Genomics, Pathogen 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(métabolisme)</term><term>Interactions hôte-pathogène</term><term>Réplication virale</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cyclophilins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclophilins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiviral Agents</term><term>Cyclosporine</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Cyclophilines</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cyclophilines</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antiviraux</term><term>Ciclosporine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Host-Pathogen Interactions</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Interactions hôte-pathogène</term><term>Réplication virale</term></keywords></textClass></profileDesc></teiHeader><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></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Perlman, S" uniqKey="Perlman S">S. Perlman</name></author><author><name sortKey="Netland, J" uniqKey="Netland J">J. Netland</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Namy, O" uniqKey="Namy O">O. Namy</name></author><author><name sortKey="Moran, S J" uniqKey="Moran S">S.J. Moran</name></author><author><name sortKey="Stuart, D I" uniqKey="Stuart D">D.I. Stuart</name></author><author><name sortKey="Gilbert, R J" uniqKey="Gilbert R">R.J. Gilbert</name></author><author><name sortKey="Brierley, I" uniqKey="Brierley I">I. Brierley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sawicki, S G" uniqKey="Sawicki S">S.G. 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Schang</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement><orgName><li>Université de Tokyo</li></orgName></list><tree><country name="Japon"><region name="Région de Kantō"><name sortKey="Tanaka, Yoshikazu" sort="Tanaka, Yoshikazu" uniqKey="Tanaka Y" first="Yoshikazu" last="Tanaka">Yoshikazu Tanaka</name></region><name sortKey="Sasaki, Takashi" sort="Sasaki, Takashi" uniqKey="Sasaki T" first="Takashi" last="Sasaki">Takashi Sasaki</name><name sortKey="Sato, Yuka" sort="Sato, Yuka" uniqKey="Sato Y" first="Yuka" last="Sato">Yuka Sato</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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