The molecular basis of host-cell permissiveness to herpes simplex viruses (HSV) is under intense investigation because of HSV prevalence in human disease and its potential use as an anti-cancer therapeutic. In August
Farassati et al. exposed to the HSV-1 virus (strain F) parental Swiss mouse embryo fibroblasts (NIH-3T3 cells) and NIH-3T3 cells transformed with the oncogenes v-erbB, sos or ras — all activators of the Ras signalling pathway. Permissiveness to HSV-1 infection (assessed by induction of cytopathic effects, viral protein synthesis and virus output) was significantly increased in NIH-3T3 cells transformed with Ras activators. In addition inhibitors of the Ras signalling pathway, such as farnesyl transferase inhibitor 1 and PD98059, effectively suppressed HSV-1 infection of ...