Figure 1

(A) Representative* list of cellular/viral protein interactions involved in RNA virus-related oncogenic transformation; (B) Schematic representation of Tax and HBZ roles in HTLV-1 mediated oncogenesis. Tax modulates the expression of many viral and cellular genes and it also promotes malignant transformation through disruption of different host-cell growth control pathways, resulting in aberrant cell division. Moreover, Tax adversely influences cellular homeostasis through a number of mechanisms, including the physical interaction with cell-cycle regulators and transcriptional activation of cell-cycle control genes, leading to uncontrolled cell division and proliferation. The basic leucine zipper protein (HBZ) is encoded by the complementary strand of the HTLV-1 genome, and it is expressed in all ATL cells, where it is capable of promoting cell proliferation and suppressing Tax-mediated transactivation. LTR: Long Terminal Repeat; NFκB: Nuclear Factor kappa-light-chain-enhancer of activated B cells; MHC-I: Major Histocompatibility Complex Class-I; STAT-5: Signal Transducer and Activator of Transcription-5; hTERT: human Telomerase Reverse Transcriptase. *Additional cellular/viral interactions involved in cell transformation and oncogenetic mechanisms have been described. This list is representative, not exhaustive.