Human Cytomegalovirus Latency: Targeting Differences in the Latently Infected Cell with a View to Clearing Latent Infection

Figure 2

HCMV latency and reactivation. Following primary infection, latency is established in the myeloid progenitor CD34+ cells which reside in the bone marrow. Viral genome is associated with chromatin markers of repression in these cells. In particular the major immediate early promoter (MIEP) is associated with a high number of cellular transcriptional repressors and a low number of cellular transcriptional activators [2–4, 34–38]. This is likely to be facilitated by an absence of the viral activator pp71 [39] concomitant with the presence of long noncoding RNA (lnr) 4.9 which is thought to interact with the polycomb repressor complex to inhibit transcription [40]. Following differentiation along the myeloid lineage of CD34+ cells into dendritic cells (DCs), the chromatin structure at the MIEP becomes associated with cellular activators of transcription and immediate early gene expression is induced and reactivation of the virus occurs [36, 37, 41].