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 Giordani, N. V.
Right arrow Articles by Bloom, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Giordani, N. V.
Right arrow Articles by Bloom, D. C.

 Previous Article  |  Next Article 

Journal of Virology, June 2008, p. 6056-6060, Vol. 82, No. 12
0022-538X/08/$08.00+0     doi:10.1128/JVI.02661-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

During Herpes Simplex Virus Type 1 Infection of Rabbits, the Ability To Express the Latency-Associated Transcript Increases Latent-Phase Transcription of Lytic Genes{triangledown}

Nicole V. Giordani,1 Donna M. Neumann,2 Dacia L. Kwiatkowski,1 Partha S. Bhattacharjee,2 Peterjon K. McAnany,1 James M. Hill,2 and David C. Bloom1*

Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida,1 Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, Louisiana2

Received 14 December 2007/ Accepted 27 March 2008

Trigeminal ganglia (TG) from rabbits latently infected with either wild-type herpes simplex virus type 1 (HSV-1) or the latency-associated transcript (LAT) promoter deletion mutant 17{Delta}Pst were assessed for their viral chromatin profile and transcript abundance. The wild-type 17syn+ genomes were more enriched in the transcriptionally permissive mark dimethyl H3 K4 than were the 17{Delta}Pst genomes at the 5' exon and ICP0 and ICP27 promoters. Reverse transcription-PCR analysis revealed significantly more ICP4, tk, and glycoprotein C lytic transcripts in 17syn+ than in 17{Delta}Pst. These results suggest that, for efficient reactivation from latency in rabbits, the LAT is important for increased transcription of lytic genes during latency.


* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, Box 100266, University of Florida College of Medicine, Gainesville, FL 32610-0266. Phone: (352) 392-8520. Fax: (352) 392-3133. E-mail: dbloom{at}ufl.edu

{triangledown} Published ahead of print on 9 April 2008.


Journal of Virology, June 2008, p. 6056-6060, Vol. 82, No. 12
0022-538X/08/$08.00+0     doi:10.1128/JVI.02661-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Whitlow, Z. W., Kristie, T. M. (2009). Recruitment of the Transcriptional Coactivator HCF-1 to Viral Immediate-Early Promoters during Initiation of Reactivation from Latency of Herpes Simplex Virus Type 1. J. Virol. 83: 9591-9595 [Abstract] [Full Text]  
  • Kwiatkowski, D. L., Thompson, H. W., Bloom, D. C. (2009). The Polycomb Group Protein Bmi1 Binds to the Herpes Simplex Virus 1 Latent Genome and Maintains Repressive Histone Marks during Latency. J. Virol. 83: 8173-8181 [Abstract] [Full Text]