MULTIPLE PATHWAYS CONTROL THE REACTIVATION OF TELOMERASE IN HTLV-I-ASSOCIATED LEUKEMIA

While telomerase (hTERT) activity is absent from normal somatic cells, reactivation of hTERT expression is a hallmark of cancer cells. Telomerase activity is is required for avoiding replicative senescence and supports immortalization of cellular proliferation. Only a minority of cancer cells rely on a telomerase-independent process known as alternative lengthening of telomeres, ALT, to sustain cancer cell proliferation. Multiple genetic, epigenetic, and viral mechanisms have been found to deregulate telomerase gene expression increasing the risk of cellular transformation. Here, we review the different strategies used by the Human T cell leukemia virus type 1, HTLV-I, to activate hTERT expression and stimulate its enzymatic activity in virally-infected CD4 T cells. The implications of hTERT reactivation in HTLV-I pathogenesis and disease treatment are discussed.