PML and infection: This nuclear host defence to infection is counteracted by the HSV-1 ubiquitin ligase ICP0 [30–32], which induces the proteasome-dependent degradation of PML (the major scaffolding protein of PML-NBs [33]), leading to the dispersal of repressive PML-NB host factors from vDNA that stimulates the progression of viral transcription and onset of lytic infection [31,32,34–37].