The innate immune DNA sensor IFI16 is in association with H3K9 methyltransferases SUV39H1 and GLP under physiological conditions in the nucleus which facilitates the epigenetic silencing of foreign viral DNA.

Inactivation of KAP1 by mTOR-mediated phosphorylation releases human cytomegalovirus from latency, and has the potential to be used as a therapy to purge the virus from transplant organs.

KSHV nullifies hypoxic restriction of DNA replication.

SND1 has m6A-reading ability and is essential for Kaposi's sarcoma-associated lytic replication.

HOIL-1 deficiency in mice results in a severe immunodeficiency that is effectively complemented by chronic infection with a murine gamma-herpesvirus.

The first structures of Kaposi’s sarcoma-associated herpesvirus ORF68 and Epstein–Barr virus BFLF1, conserved and essential proteins required in herpesviruses, reveal new insights into viral genome packaging.

Viral infection can induce NKG2D ligand expression through the action of virally encoded histone deacetylase (HDAC) inhibitors, which release HDAC mediated repression of NKG2D ligands.

The birth of the antiviral gene APOBEC3B in ancient primates is linked to the evolution of a potent counterdefense by herpesviruses, a host-pathogen interaction maintained to present day.

The human cytomegalovirus (HCMV) interactome systematically characterises high-confidence viral-viral and viral-host protein interactions in HCMV-infected cells, facilitating multiple novel insights into HCMV and herpesviral function.

Distinct binding of viral proteins to the same region on the nucleosome surface can result in contrasting changes to higher-order chromatin structure in the host cell.