Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 23, Pages 13248-13253Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01569-07
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Funding
- NEI NIH HHS [F32 EY016316, R01 EY006311, R01EY006311, P30EY002377, P30 EY002377, F32EY016316] Funding Source: Medline
- NIAID NIH HHS [AI07110, AI48633, T32 AI007110, R01 AI048633] Funding Source: Medline
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During herpes simplex virus type 1 (HSV-1) latency in mouse dorsal root ganglia (DRG), chromatin associated with the latency-associated transcript (IAT) 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 butyeate 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 0.5 111 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.
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