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 Brukman, A.
Right arrow Articles by Enquist, L. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brukman, A.
Right arrow Articles by Enquist, L. W.

 Previous Article  |  Next Article 

Journal of Virology, November 2006, p. 10871-10873, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.01308-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Pseudorabies Virus EP0 Protein Counteracts an Interferon-Induced Antiviral State in a Species-Specific Manner{triangledown}

Alla Brukman and L. W. Enquist*

Department of Molecular Biology, Princeton University, Princeton, New Jersey

Received 21 June 2006/ Accepted 11 August 2006

Pseudorabies virus (PRV), an alphaherpesvirus related to herpes simplex virus type 1 and varicella-zoster virus, infects a broad host range of mammals. A striking characteristic of PRV infection is the different symptoms and outcomes of infection in natural and nonnatural hosts. Adult pigs, the natural hosts of PRV, survive infection with only mild respiratory symptoms, while nonnatural hosts, including rodents and cattle, invariably die after exhibiting neurological symptoms. Here, we show that the PRV EP0 protein is necessary to overcome an interferon-mediated antiviral response in primary cells from the natural host of PRV but is not necessary in nonnatural-host cells.

* Corresponding author. Mailing address: Department of Molecular Biology, Princeton University, Princeton, NJ 08544. Phone: (609) 258-2415. Fax: (609) 258-1035. E-mail: lenquist{at}princeton.edu.

{triangledown} Published ahead of print on 23 August 2006.

Journal of Virology, November 2006, p. 10871-10873, Vol. 80, No. 21
0022-538X/06/$08.00+0     doi:10.1128/JVI.01308-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Saira, K., Chowdhury, S., Gaudreault, N., da Silva, L., Henderson, G., Doster, A., Jones, C. (2008). The Zinc RING Finger of Bovine Herpesvirus 1-Encoded bICP0 Protein Is Crucial for Viral Replication and Virulence. J. Virol. 82: 12060-12068 [Abstract] [Full Text]  
  • Everett, R. D., Young, D. F., Randall, R. E., Orr, A. (2008). STAT-1- and IRF-3-Dependent Pathways Are Not Essential for Repression of ICP0-Null Mutant Herpes Simplex Virus Type 1 in Human Fibroblasts. J. Virol. 82: 8871-8881 [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»