At the cellular level, gammaherpesvirus infection encompasses two broadly defined outcomes: productive, lytic replication and non-productive, latent infection. During lytic replication, viral DNA is amplified and host cell machinery is utilized for the production of viral progeny. Viral genes are actively transcribed and translated, contributing to new virus production. Ultimately, the cell is lysed and infectious virus released. In light of the fact that this process occurs quickly (24 to 48 hours in vitro) our understanding of virus-host interactions during primary infection is quite limited. During latency, viral DNA is not amplified, but instead is maintained as a nuclear episome in latently infected cells, and little viral gene transcription occurs. Latently infected cells remain intact and do not produce new infectious virus. Furthermore, it is thought that these long-lived latent cells may serve as the major mechanism by which gammaherpesviruses promote life-long infection of their hosts.