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Journal of Virology, December 2007, p. 13248-13253, Vol. 81, No. 23
0022-538X/07/$08.00+0     doi:10.1128/JVI.01569-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

In Vivo Changes in the Patterns of Chromatin Structure Associated with the Latent Herpes Simplex Virus Type 1 Genome in Mouse Trigeminal Ganglia Can Be Detected at Early Times after Butyrate Treatment

Department of Ophthalmology (LSU Eye Center of Excellence),¹ Neuroscience Center,² Department of Microbiology,³ Department of Pharmacology, Louisiana State University Health Sciences Center, New Orleans, Louisiana,⁵ Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida⁴

Received 18 July 2007/ Accepted 7 September 2007

During herpes simplex virus type 1 (HSV-1) latency in mouse dorsal root ganglia (DRG), chromatin associated with the latency-associated transcript (LAT) region of the viral genome is hyperacetylated at lysines 9 and 14 of histone 3 [H3(K9, K14)], while lytic genes are hypoacetylated. Explanted DRG exhibit a pattern of deacetylation of the LAT enhancer followed by acetylation of the ICP0 promoter at early times postexplant. Recently, we reported that sodium butyrate induced in vivo reactivation of HSV-1 in latent mice. In this study, we assessed the effect of sodium butyrate on the chromatin patterns of latent and butyrate-treated mouse trigeminal ganglia (TG) via chromatin immunoprecipitation (ChIP). We detected deacetylation of acetyl H3(K9, K14) of the LAT promoter and LAT enhancer regions as early as 0.5 h post-butyrate treatment, and this deacetylation corresponded to an increase in the acetylation of the lytic promoters ICP0 and ICP4 at 0.5 h and 1 h post-butyrate treatment, respectively. This is the first study to combine in vivo reactivation with the examination of the HSV-1 genome through ChIP assays at early times after the introduction of in vivo reactivation stimuli.

Published ahead of print on 19 September 2007.