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Journal of Virology, February 2006, p. 2063-2068, Vol. 80, No. 4
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.4.2063-2068.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Deacetylation of the Herpes Simplex Virus Type 1 Latency-Associated Transcript (LAT) Enhancer and a Decrease in LAT Abundance Precede an Increase in ICP0 Transcriptional Permissiveness at Early Times Postexplant

Antonio L. Amelio,{dagger} Nicole V. Giordani,{dagger} Nicole J. Kubat, Jerome E. O'Neil, and David C. Bloom*

Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida 32610-0266

Received 6 September 2005/ Accepted 22 November 2005

Only the latency-associated transcript (LAT) of the herpes simplex virus type 1 (HSV-1) genome is transcribed during latency, while the lytic genes are suppressed, possibly by LAT antisense mechanisms and/or chromatin modifications. In the present study, latently infected dorsal root ganglia were explanted to assess both relative levels of LAT and histone H3 (K9, K14) acetylation of the LAT locus and ICP0 promoter at early times postexplant. We observed that a decrease in both LAT enhancer histone H3 (K9, K14) acetylation and LAT RNA abundance occurs prior to an increase in acetylation, or transcriptional permissiveness, at the ICP0 promoter.

* 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.

{dagger} A.L.A. and N.V.G. contributed equally to this work.

Journal of Virology, February 2006, p. 2063-2068, Vol. 80, No. 4
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.4.2063-2068.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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