DNA viruses have long served as model systems to elucidate various aspects of eukaryotic gene regulation, due to their ease of manipulation and relatively low complexity of their genomes. In some cases, these viruses have revealed mechanisms that are subsequently recognized to apply also to cellular genes. In other cases, viruses adopt mechanisms that prove to be exceptions to the more general rules. The double-stranded DNA viruses that replicate in the eukaryotic nucleus typically utilize the host cell RNA polymerase II (RNAP II) for viral gene expression. As a consequence, these viruses must reckon with the impact of chromatin on active transcription and replication. Unlike the small DNA tumor viruses, such as polyomaviruses and papillomaviruses, the relatively large genomes of herpesviruses are not assembled into nucleosomes in the virion and stay predominantly free of histones during lytic infection. In contrast, during latency, the herpesvirus genomes associate with histones and become nucleosomal, suggesting that regulation of chromatin per se may play a role in the switch between the two stages of infection, a long-standing puzzle in the biology of herpesviruses. In this review we will focus on how chromatin formation on the herpes simplex type-1 (HSV-1) genome is regulated, citing evidence supporting the hypothesis that the switch between the lytic and latent stages of HSV-1 infection might be determined by the chromatin state of the HSV-1.