The prevalence of herpes simplex virus type 2 (HSV-2) infections in the US has increased approximately 30%. Like HSV-1, which causes facial lesions, HSV-2 causes symptomatic lesions (at genital sites) and establishes latent infections of the sensory ganglia. However, the two viruses are biologically distinct, suggesting that they possess unique functions which are mediated by different viral genes. Unlike HSV-1, HSV-2 is a tumor virus. It causes neoplastic transformation of cultured human cells and tumors in animals. The oncogene is at the 5'-terminal of a chimeric gene that also codes for the large subunit of viral ribonucleotide reductase (RR1). It was captured from the cell and it codes for a novel growth factor receptor serine-threonine protein kinase (PK) the minimal genetic information of which can adapt to a relatively wide functional diversity due to the flexibile use of additional and alternate catalytic sites and protein interaction motifs which are organized in an efficient, almost superimposed fashion. By contrast to other growth factor receptor serine-threonine kinases studied so far, the HSV-2 oncoprotein (RR1 PK) activates the RAS signaling pathway, thereby providing a biological bridge to the tyrosine growth factor receptor kinases. Expression of the oncogene is required for neoplastic transformation and tumor growth in vivo is inhibited by antisense inhibition of oncogene expression. The virus conserved the captured oncogene because it provides a biological advantage for its survival. In cultured cells, RR1 PK is required for viral IE gene transcription. In vivo, RR1 PK is likely to be involved in latency reactivation.