Epigenetic restriction of herpes simplex virus occurs in a biphasic manner, in which ATRX maintains viral heterochromatin after an initial phase of chromatin deposition.

Herpes simplex virus reactivates from a latent infection when neurons become hyperexcitable in response to an inflammatory cytokine known to be released during fever and stress.

A combination of detailed sampling and mathematical modeling suggests that the response of immune cells to reactivation of herpes simplex virus 2 is extremely rapid and effective within microscopic areas of genital skin.

Herpes simplex virus evades the immune response by inhibiting the TAP transporter with a peptide inhibitor ICP47 that has an extensive interface at the peptide translocation cavity and locks the transporter in an inactive state.

An attenuated Herpes simplex type 2 virus deleted in glycoprotein D can be used as an effective vaccine to provide robust transferable humoral immunity and complete protection in murine intravaginal and skin infection models.

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

Single-cell analyses of cells infected by Herpes Simplex Virus 1 revealed extreme heterogeneity among infected cells, including the robust activation of developmental gene programs in highly infected cells.

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.

Transient DNA interactions by DNA-binding proteins are utilized by herpes simple virus as an alternative route to generate membraneless compartments in the nucleus without invoking phase separation.

Type I IFN is a key determinant of pathogenic neutrophil activity and drives tissue pathology through modulation of IL-18 levels during genital HSV infection.