| dc.contributor.author | Ströher, U | |
| dc.contributor.author | DiCaro, A | |
| dc.contributor.author | Li, Y | |
| dc.contributor.author | Strong, JE | |
| dc.contributor.author | Aoki, F | |
| dc.contributor.author | Plummer, F | |
| dc.contributor.author | Jones, SM | |
| dc.contributor.author | Feldmann, H. | |
| dc.date.accessioned | 2013-11-27T16:06:50Z | |
| dc.date.available | 2013-11-27T16:06:50Z | |
| dc.date.issued | 2004-04 | |
| dc.identifier.citation | H. J Infect Dis. 2004 Apr 1;189(7):1164-7. Epub 2004 Mar 12. | en |
| dc.identifier.uri | http://www.ncbi.nlm.nih.gov/pubmed/15031783 | |
| dc.identifier.uri | http://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/60859 | |
| dc.description.abstract | Current treatment schemes for severe acute respiratory syndrome (SARS) include broad-spectrum antibiotics, glucocorticoids, and ribavirin. We evaluated the susceptibility of the SARS-related coronavirus (SARS CoV) to ribavirin and interferon (IFN)- alpha in vitro by use of cytopathic effect, plaque assay, and immunoblot analysis. Ribavirin did not inhibit viral growth at concentrations attainable in human serum. In contrast, IFN- alpha showed an in vitro inhibitory effect starting at concentrations of 1000 IU/mL. In conclusion, ribavirin alone is unlikely to be beneficial in the prophylaxis or treatment of SARS CoV infections. Clinical trials with IFN- alpha might be justified to determine a beneficial effect on the outcome of SARS. | en |
| dc.language.iso | en | en |
| dc.publisher | University of Nairobi | en |
| dc.title | Severe acute respiratory syndrome-related coronavirus is inhibited by interferon- alpha | en |
| dc.type | Article | en |
| local.publisher | Department of Medical Microbiology, University of Manitoba, | en |
