For HSV-1 infection, GR stimulates productive infection in neuron-like cells via GR response elements in the ICP0 promoter, and GR has also been shown to stimulate the activity of promoters driving expression of BoHV-1 bICP0 and bICP4, where the latter is a homolog of PRV IE180 (13, 27, 60). Here, NR3C1 is linked to infection.