C. M. O'Connor

This study shows CTCF binding to the HCMV MIE locus maintains latency by enabling chromatin looping that represses transcription, which is lost during reactivation.

This study shows virion-associated US28 modulates Akt activity to suppress HCMV lytic replication in monocytes, enabling quiescent infection.

This study identifies AP-1 transactivation of the MIE enhancer as critical for HCMV reactivation from latency, showing its role in de-repressing viral transcripts and downstream genes.

This study shows US28 is required for HCMV latency, independent of US27 and US29 gene expression, using mutant viruses in hematopoietic cells.

This study identifies that US28 downregulates interferon-inducible genes during HCMV latency, with IFI16 suppression enhancing viral gene expression via NF-κB.

This paper shows that the HCMV-encoded US28 receptor promotes latency by reducing c-fos expression and AP-1 binding to the MIEP.