Abstract
Herpes simplex virus (HSV) has a complicated life cycle including stages of primary lytic infection, latent infection, and reactivation. Although the HSV genomic DNA within the viral capsid is devoid of histones, it rapidly associates with histones upon entering the nucleus to form viral chromatin. This chromatin is not integrated into the host chromosome and displays features distinct from the cellular chromatin. The composition, structure, and post-translational modifications of the HSV chromatin change over the course of infection due to the actions of numerous viral and host molecules. In turn, the chromatin states influence the transcription profiles of viral genes at all stages of the viral life cycle and may dictate the outcomes of the lytic-latent balance. These mechanisms may be exploited to develop new antiviral therapeutics. This review summarizes current knowledge about the formation, regulation, and functions of the HSV chromatin and discusses the questions remaining to be answered.