gms | German Medical Science

International Conference on SARS - one year after the (first) outbreak

08. - 11.05.2004, Lübeck

Article

Send article

Search for SARS therapy

Talk

Search Medline for

  • Jindrich Cinatl jr. - Inst. f. Med. Virologie, Klinikum der J.W. Goethe-Universität, Frankfurt am Main, Germany
  • Martin Michaelis - Inst. f. Med. Virologie, Klinikum der J.W. Goethe-Universität, Frankfurt am Main, Germany
  • presenting/speaker Hans Wilhelm Doerr - Inst. f. Med. Virologie, Klinikum der J.W. Goethe-Universität, Frankfurt am Main, Germany

International Conference on SARS - one year after the (first) outbreak. Lübeck, 08.-11.05.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04sars9.01

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/sars2004/04sars046.shtml

Published: May 26, 2004

© 2004 Cinatl jr. et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

We tested a number of commercially available compounds with proven antiviral, antitumour, and /or immunosuppressive activity for their influence on SARS-Coronavirus (SCV) replication. Glycyrrhizin inhibited SCV infection at different steps of virus infectious cycle. Of twelve structurally modified glycyrrhizin derivatives, two were found to be about 10-fold more potent than the parental drug. Ribavirin inhibited SCV replication in MA-104 and Caco-2 cells but not in Vero cells at clinical achievable concentrations (5-50 µg/ml). Type I interferons (IFNs) (α, β) had a higher anti-SCV activity than IFN-γ, with IFN-β being the most effective IFN. Combination of IFN-β and ribavirin inhibited SCV replication synergistically. Hydrocortisone did not influence SCV replication. However, high concentrations of hydrocortisone reverted SCV-induced up-regulation of proinflammatory genes and prevented activation of proinflammatory transcription factors.