Combining integrative genomics and systems biology approaches has revealed new and conserved features in the genome of human herpesvirus 6.

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

Rodent herpesvirus Peru overcomes NK ‘missing-self’ killing using a non-classical MHC-I like protein resistant todownregulation by its own ubiquitin ligase that potently sabotages antigen presentation to T-cells.

Unbiased mapping of viral open reading frames (ORFs) and transcripts in HHV-6 genomes uncovers novel ORFs and lncRNAs that are conserved across betaherpesviruses.

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.

A conserved viral protein complex that promotes membrane wrapping of nascent herpesvirus particles shows structural similarity to cellular membrane-remodelling proteins, suggesting functional mimicry.

Internal DNA pressure of tens of atmospheres inside a herpesvirus capsid powers ejection of the viral genome into a cell nucleus, causing infection.

A herpesvirus harnesses the unfolded protein response to regulate its own life cycle, revealing an unexpected role of XBP1u as a potent repressor of the most important viral promoter.

CRISPR genome editing technology can efficiently introduce mutations into lytic and latent HSV genomes to block lytic replication and reactivation of latent herpes simplex virus genome though differential mechanisms.

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