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 Larsen, R.
Right arrow Articles by Robertsen, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Larsen, R.
Right arrow Articles by Robertsen, B.

 Previous Article  |  Next Article 

Journal of Virology, August 2004, p. 7938-7944, Vol. 78, No. 15
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.15.7938-7944.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Inhibition of Infectious Pancreatic Necrosis Virus Replication by Atlantic Salmon Mx1 Protein

Rannveig Larsen, Torunn P. Røkenes, and Børre Robertsen*

Department of Marine Biotechnology, Norwegian College of Fishery Science, University of Tromsø, N-9037 Tromsø, Norway

Received 15 December 2003/ Accepted 1 April 2004

Mx proteins form a family of interferon (IFN)-induced GTPases with potent antiviral activity against various single-stranded RNA viruses in mammals and chickens. In fish, alpha/beta IFN has been reported to inhibit the replication of infectious pancreatic necrosis virus (IPNV), but the mode of action has not been elucidated. A correlation between the inhibition of IPNV and Mx protein expression has, however, been observed. To examine whether Atlantic salmon Mx1 protein (ASMx1) possesses antiviral activity against IPNV, CHSE-214 cells constitutively expressing ASMx1 were established. ASMx1 appeared to be localized in the cytoplasm. The ASMx1-expressing clone selected showed a severely reduced IPNV-induced cytopathic effect, which was confirmed by a 500-fold reduction in virus yield. The antiviral activity against IPNV was further confirmed by the inhibition of virus protein synthesis and the reduced accumulation of virus transcripts. The present work further adds to the body of evidence which suggests that antiviral activity is a major functional role of vertebrate Mx proteins. Moreover, the list of viruses inhibited by Mx proteins is extended to include double-stranded RNA viruses.

* Corresponding author. Mailing address: Norwegian College of Fishery Science, University of Tromsø, N-9037 Tromsø, Norway. Phone: 47 77 64 44 87. Fax: 47 77 64 60 20. E-mail: borrer{at}nfh.uit.no.

Journal of Virology, August 2004, p. 7938-7944, Vol. 78, No. 15
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.15.7938-7944.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Pedersen, T., Skjesol, A., Jorgensen, J. B. (2007). VP3, a Structural Protein of Infectious Pancreatic Necrosis Virus, Interacts with RNA-Dependent RNA Polymerase VP1 and with Double-Stranded RNA. J. Virol. 81: 6652-6663 [Abstract] [Full Text]  
  • Wong, R. T.-Y., Hon, C.-C., Zeng, F., Leung, F. C.-C. (2007). Screening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays. J. Gen. Virol. 88: 1785-1796 [Abstract] [Full Text]  
  • Mundt, E. (2007). Human MxA protein confers resistance to double-stranded RNA viruses of two virus families. J. Gen. Virol. 88: 1319-1323 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»