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

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.

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.

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.

In a study of a herpes simplex virus (HSV) vaccine, the combination of sex and prior exposure to the virus resulted in HSV naive women mounting a prominent type I interferon response associated with reduced neutralizing titers to HSV.

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.

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

Characterization of PML subnuclear structures during human cytomegalovirus infection demonstrates that prolonged interferon and DNA damage signaling can induce giant PML nuclear bodies which sequentially entrap both nucleic acids and viral proteins as a cytoprotective mechanism.

Herpes simplex ICP4 preferentially binds to and delineates the viral genome, ultimately resulting in robust viral transcription at the expense of the host.

Interactions were visualized between the nuclear egress complex from herpes simplex virus and a capsid protein that could promote nucleocytoplasmic translocation of the capsid in infected cells.