Release of Human Cytomegalovirus from latency by a KAP1/TRIM28 phosphorylation switch. Homo sapiens

A new actor of HCMV latency is unveiled, where KAP1 protein binds to viral genome to recruit SetDB1 and trigger H3K9 trimethylation. A switch of phosphorylation state mediated by mTOR leads to lytic replication, opening new approaches to curtail CMV infection but also to purge the virus from organ transplants. Overall design: Analyses of transcriptional profiles and chromatin state in KAP1 WT and KO (or KD) cells