Oncogenic viruses provide their host cells with additional growth stimuli, thereby extending their proliferative capacity. This implies that viral oncogenes can override growth-suppressive signals, which control cell-cycle progression in untransformed cells. Viral oncoproteins deregulate cell-cycle control by interfering with receptor-mediated signal transduction pathways and the function of nuclear cell-cycle regulatory proteins. As a consequence of these regulatory interactions, many viral oncogenes induce the expression of cellular genes required for cell-cycle progression, including genes encoding G1 cyclins. Apparently, different oncogenic viruses target different subsets of these cell-cycle regulatory pathways to transform cells.