Ian J. Groves

This study shows that deletion of UL33 from HCMV genome reduces lytic replication in epithelial cells by impairing Gq-dependent signaling and gene expression.

This study identifies UL78 as a viral factor that facilitates the switch from latency to reactivation in CMV-infected myeloid cells by modulating cellular signaling.

This study shows that deleting a CTCF-binding site upstream of the Epstein-Barr virus C-promoter increases Cp transcription and EBNA2 recruitment, while other promoters are downregulated.