To establish an infection, viruses need to suppress a number of host immune responses, the antiviral activity induced by IFNs, the chemotaxis of immune cells induced by chemokines/cytokines, the maturation and activation of DCs, activation of NK and NKT cells, transmigration of mature DCs to the lymph nodes, and the differentiation and activation of T cells and B cells in the lymph nodes, for example. When viruses infect immune cells, such as DCs, the infected cells frequently show suppression of maturation and differentiation, suppression of cytokine receptor and costimulatory molecule expression, secretion of molecules that mimic cytokines and cytokine receptors, and so on. Furthermore, infected cells often alter their cytokine profiles. These strategies are used by the virus to inhibit the acquired immune response. In addition, it has been suggested that virus infection induces regulatory T cells. Type 1 (HTLV-1) . HTLV-1, which is a retrovirus, infects CD4 + T lymphocytes, CD8 + T lymphocytes, DCs, B cells, macrophages, and astrocytes, and preferentially replicates in CD4 + T lymphocytes. HTLV-1 causes latent infection as a provirus, whose genome is integrated into the host DNA, and does not replicate in cells in G0 phase. When the infected T lymphocytes are stimulated with antigen presentation from DCs, they proliferate triggering HTLV-1 replication. During the replication stage, a viral protein, Tax, activates NF-κB and promotes the growth of infected cells via upregulation of IL-2 and IL-2 receptors [6, 7] . NF-κB also activates the long terminal repeat (LTR) of HTLV-1 genome, which further enhances viral replication [8] . The replicated virus induces a host immune response, and cells infected with virus are eliminated by the induction of cytotoxic T cells specific for HTLV-1 Tax. In patients with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), the high proviral load induces a strong HTLV-1-specific immune response [9] . This leads to the rapid elimination of infected cells through the induction of proinflammatory cytokines and cytotoxic T lymphocytes. So, in order to escape from acquired immune responses, HTLV-1 needs minimum replication and latent infection.