Transactivation by the herpes simplex virus virion protein Vmw65 and viral permissivity in a neuronal cell line with reduced levels of the cellular transcription factor Oct-1.

Transactivation of the herpes simplex virus (HSV) immediate-early (IE) genes is dependent upon the formation of a complex between the viral protein Vmw65 and the cellular transactivation factor Oct-1. Differentiation of the proliferating ND7 neuronal cell to a nondividing phenotype results in a large fall in the amount of Oct-1 to a level characteristic of nondividing neuronal cells but does not dramatically affect the level of IE gene expression following infection or the ability of Vmw65 to transactivate the IE promoter in transfection experiments. This suggests that the low levels of Oct-1 in nonproliferating neuronal cells do not play a key role in the failure of IE gene expression following initial infection of these cells, which is an essential step in the establishment of latent infections with HSV.