Herpes simplex virus 1 (HSV-1) is a highly prevalent DNA virus with a major impact on human health. The HSV-1 genome is assembled into stable chromatin and minimally transcribed during latent infection in neurons or assembled into highly dynamic chromatin and highly transcribed during lytic infection in non-neuronal cells. It is unclear how HSV-1 genomes transition from static to highly dynamic chromatin during reactivation, but epigenetics and chromatin dynamics have been proposed to play an important role. Chromatin remodeling complexes regulate cellular chromatin dynamics and contribute to DNA transcription, replication, and repair. The BAF family of chromatin remodeling complexes includes three ubiquitously expressed complexes (cBAF, PBAF, and GBAF) and cell type-specific complexes, including a neuronal BAF (nBAF). In this thesis, I explore the roles of BAF complexes throughout HSV-1 infection. In lytic infection in non-neuronal cells, three subunits shared by all BAF complexes and a unique subunit each from cBAF, PBAF, and GBAF were enriched in herpes nuclear domains (HND), which are the novel nuclear domains formed during lytic infection in which HSV-1 genomes are transcribed, replicated, and packaged. The ATPase SMARCA4, which is shared by all BAF complexes, bound HSV-1 genomes. Four structurally unrelated small molecule bromodomain inhibitors of BAF complexes modulated abundance of some HSV-1 transcripts, but not genome copy numbers. The inhibitors did not inhibit the recruitment of BAF subunits to HND, and four commonly acetylated histone residues were depleted from HND. In neuronal cells, BAF subunits colocalize with active and latent HSV-1 genomes. In a pilot experiment, treatment with small molecule inhibitors of BAF bromodomains or ATPase domains induced reactivation of latent HSV-1 genomes. We propose BAF complexes are differentially recruited to HND through VP16 and ICP8, independently of their bromodomains. BAF complexes remodel HSV-1 chromatin, inhibiting viral transcription prior to the onset of DNA synthesis.