This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ali, S.
Right arrow Articles by Kukolj, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ali, S.
Right arrow Articles by Kukolj, G.

 Previous Article  |  Next Article 

Journal of Virology, March 2005, p. 3174-3178, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.3174-3178.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Interferon Regulatory Factor 3-Independent Double-Stranded RNA-Induced Inhibition of Hepatitis C Virus Replicons in Human Embryonic Kidney 293 Cells

Samir Ali and George Kukolj*

Department of Biological Sciences, Boehringer Ingelheim Canada Ltd., Research and Development, Laval, Quebec, Canada

Received 20 July 2004/ Accepted 19 October 2004

The treatment of human embryonic kidney 293 cells harboring a hepatitis C virus (HCV) subgenomic replicon with the double-stranded RNA (dsRNA) mimic poly(I · C) inhibits HCV RNA replication through an undefined mechanism. Interferon regulatory factor 3 (IRF 3) has been widely postulated to mediate various antiviral responses, and its role in mediating the response to dsRNA in 293 cells was examined. Treating the cells with dsRNA did not induce IRF-3 activation, as measured by nuclear localization or the induction of reporter genes. Moreover, the expression of a dominant negative form of IRF-3 did not affect either colony formation upon transfection of subgenomic replicon RNA or the inhibition of the HCV replicon by dsRNA. Our results suggest that the inhibition of HCV RNA replication by poly(I · C) in 293 cells is independent of IRF-3 activation.


* Corresponding author. Mailing address: Boehringer Ingelheim Canada Ltd. R&D, Biological Sciences, 2100 rue Cunard, Laval, Quebec H7S 2G5, Canada. Phone: (450) 682-4640. Fax: (450) 682-4642. E-mail: gkukolj{at}lav.boehringer-ingelheim.com.


Journal of Virology, March 2005, p. 3174-3178, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.3174-3178.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • DeWitte-Orr, S. J., Mehta, D. R., Collins, S. E., Suthar, M. S., Gale, M. Jr., Mossman, K. L. (2009). Long Double-Stranded RNA Induces an Antiviral Response Independent of IFN Regulatory Factor 3, IFN-{beta} Promoter Stimulator 1, and IFN. J. Immunol. 183: 6545-6553 [Abstract] [Full Text]  
  • Chang, K.-S., Cai, Z., Zhang, C., Sen, G. C., Williams, B. R. G., Luo, G. (2006). Replication of Hepatitis C Virus (HCV) RNA in Mouse Embryonic Fibroblasts: Protein Kinase R (PKR)-Dependent and PKR-Independent Mechanisms for Controlling HCV RNA Replication and Mediating Interferon Activities.. J. Virol. 80: 7364-7374 [Abstract] [Full Text]