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 Liu, M.
Right arrow Articles by Vakharia, V. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, M.
Right arrow Articles by Vakharia, V. N.

 Previous Article  |  Next Article 

Journal of Virology, April 2006, p. 3369-3377, Vol. 80, No. 7
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.7.3369-3377.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

Meihong Liu and Vikram N. Vakharia*

Center for Biosystems Research, University of Maryland Biotechnology Institute, College Park, Maryland 20742

Received 2 September 2005/ Accepted 3 January 2006

Infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, carries a small nonstructural protein (NS). This protein has been implicated to play a role in the induction of apoptosis. In this study, we investigate the kinetics of viral replication during a single round of viral replication and examine the mechanism of IBDV-induced apoptosis. Our results show that it is caspase dependent and activates caspases 3 and 9. Nuclear factor kappa B (NF-{kappa}B) is also activated and is required for IBDV-induced apoptosis. The NF-{kappa}B inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-{kappa}B activation. To study the function of the NS protein in this context, we generated the recombinant rGLS virus and an NS knockout mutant, rGLSNS{Delta} virus, using reverse genetics. Comparisons of the replication kinetics and markers for virally induced apoptosis indicated that the NS knockout mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-{kappa}B activation. These results suggest that the NS protein has an antiapoptotic function at the early stage of virus infection.


* Corresponding author. Mailing address: Center for Biosystems Research, 5115 Plant Sciences Building, University of Maryland Biotechnology Institute, College Park, MD 20742. Phone: (301) 405-4777. Fax: (301) 314-9075. E-mail: vakharia{at}umbi.umd.edu.


Journal of Virology, April 2006, p. 3369-3377, Vol. 80, No. 7
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.7.3369-3377.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Poenisch, M., Burger, N., Staeheli, P., Bauer, G., Schneider, U. (2009). Protein X of Borna Disease Virus Inhibits Apoptosis and Promotes Viral Persistence in the Central Nervous Systems of Newborn-Infected Rats. J. Virol. 83: 4297-4307 [Abstract] [Full Text]  
  • Zheng, X., Hong, L., Shi, L., Guo, J., Sun, Z., Zhou, J. (2008). Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus. Mol. Cell. Proteomics 7: 612-625 [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]