Some virus proteins are known as negative regulators of replication. The HTLV-1 basic leucine-zipper factor (HBZ) protein suppresses Tax-mediated transcription activation of the viral LTR [10] . The p30 protein suppresses transcription of mRNAs encoding Tax and Rev [11] . p30 also contributes to the expression of TLR2, TLR4, and TLR9, and activation of IRF4. In monocytes, the TLR2 gene promoter is regulated by the transcription factors Sp1, Sp3, and PU.1 [12] , and the TLR4 gene by ISRE and PU.1 [13] . p30 downregulates the expression of both TLR2 and TLR4, because it binds to PU.1 and prevents it from binding to DNA [14] . This leads to the suppression of DC maturation, and of their subsequent migration to the lymph nodes. Furthermore, p30 suppresses the enzymatic activity of glycogen synthetase kinase 3β (GSK3β) through promotion of the phosphorylation of nine serine residues. This leads to the induction of IL-10, which suppresses the function of macrophages, and also the maturation and activation of DCs. In fact, serum IL-10 levels are elevated in patients with adult T lymphocyte leukemia. These immunosuppressive properties of IL-10 indirectly contribute to the inhibition of virus replication and to the suppression of virus-induced immune responses. Activation of infected T lymphocytes by DCs in the lymph nodes and cell-to-cell transmission of virus are considered to be important for virus proliferation in human. The viral p12 protein suppresses cell surface expression of both MHC class I and the IL-2 receptor, and also suppresses linker for activation of T cells (LAT), which is an adaptor protein required for T cell activation [15] . This results in suppression of T cells and dystunction of the stimulation/activation by DCs via the T cell receptor. HTLV-1 causes proliferation of infected cells rather than virus and suppression of host immune responses, which helps it to maintain a latent infection in order to survive. can infect CD4 + T lymphocytes, monocytes, macrophages, and DCs, and preferentially replicates in activated T lymphocytes and activated macrophages. It replicates generally much more slowly in DCs regardless of maturation stage.