Oncogenic viruses provide their host cells with additional growth stim
uli, thereby extending their proliferative capacity. This implies that
viral oncogenes can override growth-suppressive signals, which contro
l cell-cycle progression in untransformed cells. Viral oncoproteins de
regulate cell-cycle control by interfering with receptor-mediated sign
al transduction pathways and the function of nuclear cell-cycle regula
tory 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. Apparentl
y, different oncogenic viruses target different subsets of these cell-
cycle regulatory pathways to transform cells.