Full metadata record
DC FieldValueLanguage
dc.contributor.authorHung, Hui-Chenen_US
dc.contributor.authorShih, Shin-Ruen_US
dc.contributor.authorChang, Teng-Yuanen_US
dc.contributor.authorFang, Ming-Yuen_US
dc.contributor.authorHsu, John T. -A.en_US
dc.date.accessioned2015-07-21T11:21:01Z-
dc.date.available2015-07-21T11:21:01Z-
dc.date.issued2014-11-20en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://dx.doi.org/10.1371/journal.pone.0111331en_US
dc.identifier.urihttp://hdl.handle.net/11536/123896-
dc.description.abstractEnterovirus 71 (EV-A71) is a neurotropic virus that can cause severe complications involving the central nervous system. No effective antiviral therapeutics are available for treating EV-A71 infection and drug discovery efforts are rarely focused to target this disease. Thus, the main goal of this study was to discover existing drugs with novel indications that may effectively inhibit EV-A71 replication and the inflammatory cytokines elevation. In this study, we showed that LiCl, a GSK3 beta inhibitor, effectively suppressed EV-A71 replication, apoptosis and inflammatory cytokines production (Interleukin 6, Interleukin-1 beta) in infected cells. Furthermore, LiCl and an immunomodular agent were shown to strongly synergize with each other in suppressing EV-A71 replication. The results highlighted potential new treatment regimens in suppressing sequelae caused by EV-A71 replication.en_US
dc.language.isoen_USen_US
dc.titleThe Combination Effects of LiCl and the Active Leflunomide Metabolite, A771726, on Viral-Induced Interleukin 6 Production and EV-A71 Replicationen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0111331en_US
dc.identifier.journalPLOS ONEen_US
dc.citation.issue11en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000345253000007en_US
dc.citation.woscount0en_US
Appears in Collections:Articles


Files in This Item:

  1. 000345253000007.pdf