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Journal of Virology, January 2007, p. 59-67, Vol. 81, No. 1
0022-538X/07/$08.00+0     doi:10.1128/JVI.01171-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

A Protein Encoded by the Bovine Herpesvirus 1 Latency-Related Gene Interacts with Specific Cellular Regulatory Proteins, Including CCAAT Enhancer Binding Protein Alpha{triangledown}

Florencia Meyer, Sandra Perez, Vicki Geiser, Mark Sintek, Melissa Inman, and Clinton Jones*

Department of Veterinary and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Lincoln, Nebraska 68503

Received 6 June 2006/ Accepted 12 September 2006

Following acute infection, bovine herpesvirus 1 establishes latency in sensory neurons of trigeminal ganglia (TG). Reactivation from latency occurs periodically, resulting in the shedding of infectious virus. The latency-related (LR) RNA is abundantly expressed in TG of latently infected calves, and the expression of LR proteins is necessary for dexamethasone-induced reactivation from latency. Previously published studies also identified an alternatively spliced LR transcript which is abundantly expressed in TG at 7 days after infection and has the potential to encode a novel LR fusion protein. Seven days after infection is when extensive viral gene expression is extinguished in TG and latency is established, suggesting that LR gene products influence the establishment of latency. In this study, we used a bacterial two-hybrid assay to identify cellular proteins that interact with the novel LR fusion protein. The LR fusion protein interacts with two proteins that can induce apoptosis (Bid and Cdc42) and with CCAAT enhancer binding protein alpha (C/EBP-{alpha}). Additional studies confirmed that the LR fusion protein interacts with human or insect C/EBP-{alpha}. C/EBP-{alpha} protein expression is induced in TG neurons of infected calves and after dexamethasone-induced reactivation from latency. Wild-type C/EBP-{alpha}, but not a DNA binding mutant of C/EBP-{alpha}, enhances plaque formation in bovine cells. We hypothesize that interactions between the LR fusion protein and C/EBP-{alpha} promote the establishment of latency.

* Corresponding author. Mailing address: Department of Veterinary and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Lincoln, NE 68503. Phone: (402) 472-1890. Fax: (402) 472-9690. E-mail: cjones{at}unlnotes.unl.edu.

{triangledown} Published ahead of print on 20 September 006.

Journal of Virology, January 2007, p. 59-67, Vol. 81, No. 1
0022-538X/07/$08.00+0     doi:10.1128/JVI.01171-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Jaber, T., Henderson, G., Li, S., Perng, G.-C., Carpenter, D., Wechsler, S. L., Jones, C. (2009). Identification of a novel herpes simplex virus type 1 transcript and protein (AL3) expressed during latency. J. Gen. Virol. 90: 2342-2352 [Abstract] [Full Text]  
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