Epstein-Barr Virus (EBV) establishes latent infection as a circular, chromatinized episome that can persist in the nucleus of dividing and quiescent B cells, as well as in some NK, T, and epithelial cancer cells. During latency, the viral genome can express a diverse program of viral genes that have profound effects on the host cell, including capacity for immortalization, metabolic shifts, and immune evasion. The selective expression of viral genes during latency requires complex coordination between viral and host factors. This coordination is regulated by the chromatin structure and epigenetic programming of the viral genome. Epigenetic programming is determined by chromatin assembly, nucleosome positioning, histone and DNA modifications, transcription factor binding, RNA polymerase signaling, DNA looping, higher-ordered chromatin architecture, and interactions with host chromosome domains and territories. In addition, the latent viral genome divides using host replication and chromosome segregation machinery. Under stress conditions, the viral episome can switch into a lytic cycle where many additional viral factors are expressed to control late gene expression and viral rolling-circle replication followed by virion assembly and packaging. How the chromatin structure of the virus controls and is coordinated with all of these different processes and transitions is the focus of this chapter. Here we highlight recent advances in EBV chromatin control since the first edition of this chapter.