The oncogenic potential of herpes simplex viruses: evidence for a 'hit-and-run' mechanism.

Experiments to determine the mechanism of transformation of herpes simplex virus (HSV) have identified fragments of viral DNA which are able to initiate transformation. No set of viral genes seems to be consistently retained or expressed in the transformed cells or in human cervical tumours, suggesting that viral DNA is not needed to maintain the transformed phenotype. In fact there is no conclusive evidence that initiation of neoplasia is mediated by a viral protein. Here we revisit the 'hit-and-run' hypothesis and its implications for HSV-induced tumorigenicity.