The relative paucity of knowledge on the entry of HCMV into sites of latency is no doubt due in part to the relative difficulty of working with the primary cell types, in which HCMV establishes latent infections in vivo, which are CD34+ myeloid progenitor cells [27,28], compared to studies of lytic infection that tend to utilise primary fibroblasts or epithelial cells. The gene discussed is CD34; the disease is disease arising from reactivation of latent virus.