A model for HTLV-1-specific pathogenesis. The amounts of IL-2 or similar T-cell growth-promoting cytokines are low in vivo. In such environment, HTLV-1 infected cells proliferate more efficiently than HTLV-2 infected cells, and have greater probability to acquire genetic and/or epigenetic mutations. In addition, increased proliferation of HTLV-1 infected T-cells would effectively deteriorate the host immune system. Once such mutated cells accumulate with a reduced host immune activity, HTLV-1-infected T-cells can grow monoclonally, resulting in ATL development. For HAM/TSP, an increase in HTLV-1-infected cells in vivo induces more immune response to HTLV-1, especially to Tax1, resulting in HAM/TSP development through an autoimmune mechanism.