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 onset of lytic infection [31, 32, 34-37]. Here, PML is linked to infection.