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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: Virology. 2018 Jul 14;522:81–91. doi: 10.1016/j.virol.2018.07.011

Figure 2. Model of HSV reactivation in response to axotomy/explant.

Figure 2.

Following axotomy, there is a rapid increase in intracellular calcium levels triggering a calcium wave that is propagated to the soma. This permits rapid cellular responses, including a global increase in histone acetylation due to the export of HDAC5, along with HDAC3, from the nucleus. This may explain the increased histone acetylation observed on HSV lytic promoters following explant. Increased intracellular calcium also activates adenylate cyclase and DLK, which activates JNK. JNK activity is required for explant induced reactivation. HCF-1 has been found to rapidly translocate to the nucleus and bind to HSV IE promoters. Viral gene expression is dependent on LSD-1 and JMJD2 histone K9 demethylase activity, which are presumably recruited along with Set1, by HCF-1.