Figure 5.

Functional interactions of Tax and p13 in HTLV-1 persistence and T-cell transformation. Studies carried out so far suggest that Tax and p13 might act in concert to maintain the proliferation and survival rates of infected cells at a level compatible with long term viral persistence and survival of the host. Solid lines indicate demonstrated effects, while dotted lines indicate hypothetical interactions. Tax drives T-cell proliferation and reduces cell death resulting in the accumulation of infected cell pool; however due to the effects of Tax on cell cycle checkpoints and genetic stability these cells are prone to accumulate genetic lesions resulting in the emergence of neoplastic clones giving rise to ATLL. p13 activation of resting T-cells might cooperate with Tax in expanding the pool of “normal” infected T-cells; however, the proapototic effect of p13 on tumor cells might contrast with the anti-apoptotic effect of Tax, reducing the probability of ATLL transformation.