Genomic analyses provide new insights into natural history and pathogenesis of cytomegalovirus infection and suggest new testable hypotheses that could be important for the design and implementation of new vaccines.

The human cytomegalovirus US12 gene family work co-operatively to degrade large numbers of immune ligands and prevent recognition by natural killer cells.

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.

Single-cell and bulk expression analyses reveal that HCMV latent infection drives cells towards a weaker immune-responsive state, which is important for its expression and reactivation.

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.

Molecular mechanisms reveal that human cytomegalovirus has evolved to deploy two individual glycoproteins working in synergy to efficiently evade antibody-mediated immunity mediated by Fc-gamma receptors.

Cytomegaloviruses are recognized by distinct sensors depending on the infected cell type and together these sensors are essential for viral control and downstream immune responses.

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.

The HCMV virion envelope is derived from the host exosome membrane, and exosome machinery and export pathways facilitate virion egress.

Single mouse cytomegalovirus protein, m154, downmodulates surface expression of numerous targets important for NK and CD8 T cell activation by perturbing adaptor protein-1 sorting and redirecting targets to lysosomal degradation.