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. 2008 Jun;72(2):249–265. doi: 10.1128/MMBR.00040-07

FIG. 3.

FIG. 3.

Subcellular localization of tegument-delivered pp71 determines whether HCMV initiates lytic replication or establishes quiescent, latent-like infections. (A) Lytic replication initiates when tegument-delivered pp71 is allowed access to the nucleus. Capsids docked at nuclear pores release their DNA into the nucleus, and viral genomes associate with cellular histones (H). The Daxx protein, which rapidly dissociates from, and reassociates with, PML-NBs, accumulates around viral genomes, recruits an HDAC, and silences viral IE gene expression. Other PML-NB components are also recruited and participate in the silencing of viral genomes. pp71 binds to Daxx in these newly formed PML-NBs, induces Daxx degradation, derepresses viral IE gene expression, and thus initiates the lytic replication cycle. (B) In cells where quiescent or latent infections are established, tegument-delivered pp71 remains in the cytoplasm. Daxx (and presumably other PML-NB proteins) silences viral gene expression in these cells.