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Journal of Virology, November 2007, p. 12394-12405, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.01068-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Relaxed Repression of Herpes Simplex Virus Type 1 Genomes in Murine Trigeminal Neurons{triangledown}

Tracy Terry-Allison, Colton A. Smith,{dagger} and Neal A. DeLuca*

Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

Received 17 May 2007/ Accepted 30 August 2007

The expression of herpes simplex virus (HSV) genomes in the absence of viral regulatory proteins in sensory neurons is poorly understood. Previously, our group reported an HSV immediate early (IE) mutant (d109) unable to express any of the five IE genes and encoding a model human cytomegalovirus immediate early promoter-green fluorescent protein (GFP) transgene. In cultured cells, GFP expressed from this mutant was observed in only a subset of infected cells. The subset exhibited cell type dependence, as the fractions of GFP-expressing cells varied widely among the cell types examined. Herein, we characterize this mutant in murine embryonic trigeminal ganglion (TG) cultures. We found that d109 was nontoxic to neural cultures and persisted in the cultures throughout their life spans. Unlike with some of the cultured cell lines and strains, expression of the GFP transgene was observed in a surprisingly large subset of neurons. However, very few nonneuronal cells expressed GFP. The abilities of ICP0 and an inhibitor of histone deacetylase, trichostatin A (TSA), to activate GFP expression from nonexpressing cells were also compared. The provision of ICP0 by infection with d105 reactivated quiescent genomes in nearly every cell, whereas reactivation by TSA was much more limited and restricted to the previously nonexpressing neurons. Moreover, we found that d109, which does not express ICP0, consistently reactivated HSV type 1 (KOS) in latently infected adult TG cultures. These results suggest that the state of persisting HSV genomes in some TG neurons may be more dynamic and more easily activated than has been observed with nonneuronal cells.

* Corresponding author. Mailing address: E1257 Biomedical Science Tower, Dept. of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261. Phone: (412) 648-9947. Fax: (412) 624-1401. E-mail: ndeluca{at}pitt.edu

{triangledown} Published ahead of print on 12 September 2007.

{dagger} Present address: Skidaway Institute of Oceanography, Savannah, GA 31411.

Journal of Virology, November 2007, p. 12394-12405, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.01068-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ferenczy, M. W., DeLuca, N. A. (2009). Epigenetic Modulation of Gene Expression from Quiescent Herpes Simplex Virus Genomes. J. Virol. 83: 8514-8524 [Abstract] [Full Text]  
  • Everett, R. D., Parsy, M.-L., Orr, A. (2009). Analysis of the Functions of Herpes Simplex Virus Type 1 Regulatory Protein ICP0 That Are Critical for Lytic Infection and Derepression of Quiescent Viral Genomes. J. Virol. 83: 4963-4977 [Abstract] [Full Text]  
  • Preston, C. M., Nicholl, M. J. (2008). Induction of Cellular Stress Overcomes the Requirement of Herpes Simplex Virus Type 1 for Immediate-Early Protein ICP0 and Reactivates Expression from Quiescent Viral Genomes. J. Virol. 82: 11775-11783 [Abstract] [Full Text]  
  • Everett, R. D., Parada, C., Gripon, P., Sirma, H., Orr, A. (2008). Replication of ICP0-Null Mutant Herpes Simplex Virus Type 1 Is Restricted by both PML and Sp100. J. Virol. 82: 2661-2672 [Abstract] [Full Text]  


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