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HTLV\u20101\u2010specific T\u2010cell responses elicit antitumor and antiviral effects in experimental models, and are considered to be one of the most important determinants of the disease manifestation, since they are activated in HAM\/TSP but not in ATL patients. The combination of low T\u2010cell responses and elevated HTLV\u20101 proviral loads are features of ATL, and are also observed in a subpopulation of HTLV\u20101 carriers at the asymptomatic stage, suggesting that these features may be underlying risk factors. These risks may potentially be reduced by vaccination to activate HTLV\u20101\u2010specific T\u2010cell responses. HAM\/TSP and ATL patients also differ in their levels of HTLV\u20101 mRNA expression, which are generally low <jats:italic>in vivo<\/jats:italic> but slightly higher in HAM\/TSP patients. Our recent study indicated that viral expression in HTLV\u20101\u2010infected T\u2010cells is suppressed by stromal cells in culture through type\u2010I IFNs. The suppression was reversible after isolation from the stromal cells, mimicking a long\u2010standing puzzling phenomenon in HTLV\u20101 infection where the viral expression is very low <jats:italic>in vivo<\/jats:italic> and rapidly induced <jats:italic>in vitro<\/jats:italic>. Collectively, HTLV\u20101 is controlled by both acquired and innate immunity <jats:italic>in vivo<\/jats:italic>: HTLV\u20101\u2010specific T\u2010cells survey infected cells, and IFNs suppress viral expression. Both effects would contribute to a reduction in viral pathogenesis, although they may potentially influence or conflict with one another. The presence of double control systems for HTLV\u20101 infection provides a new concept for understanding the pathogenesis of HTLV\u20101\u2010mediated malignant and inflammatory diseases. 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