In conclusion, our data provide evidence for prolonged gammaherpesvirus infection in endothelial cells. This outcome appears to be the result of a specific interaction between cHV68 and endothelial cells, as it is promoted by a viral gene (the cHV68 v-cyclin) and, to date, is unique to endothelial cells. These data further refine the concept of gammaherpesvirus infection and demonstrate that a gammaherpesvirus can undergo robust productive replication in the context of prolonged host cell viability. Identification of intermediate outcomes of gammaherpesvirus infection, such as the one we have described here, has major implications for our understanding of the nature of gammaherpesvirus infection as it relates to specific cell types. Such a course of infection provides an additional mechanism, beyond latency, by which gammaherpesviruses can achieve longterm propagation.