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
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
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DOI：
10.1128/jvi.80.4.2063-2068.2006
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发表时间：
2006-02-01
影响因子：
5.4
通讯作者：
Bloom, DC
中科院分区：
文献类型：
--
作者：
Amelio, AL;Giordani, NV;Bloom, DC
只有潜伏相关转录本（LAT）的单纯疱疹病毒1型（HSV-1）基因组在潜伏期转录，而裂解基因被抑制，可能是通过LAT反义机制和/或染色质修饰。在本研究中，潜伏性感染的背根神经节被标记，以评估移植后早期LAT和LAT基因座和ICPO启动子的组蛋白H3（K9，K14）乙酰化的相对水平。我们观察到LAT增强子组蛋白H3（K9，K14）乙酰化和LAT RNA丰度的降低发生在ICPO启动子处乙酰化或转录允许性增加之前。
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 ICPO 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 ICPO promoter.