Abstract

Human T-cell leukemia virus type 1 (HTLV-1) only infects through cell-to-cell contact. Therefore, HTLV-1 increases the number of infected cells in vivo. Infected cells would evade the host immune responses and for its transmission, infiltrate into breast milk and semen. HTLV-1 bZIP factor (HBZ) changes the immunophenotype of infected cells to "regulatory T-cell like", which is critical for its escape from host immunosurveillance. Tax is essential for de novo infection. An immunogenic viral protein, Tax, is transiently expressed to minimize the risk of immune attack from the host. HTLV-1 causes oncogenesis and inflammation, both of which are closely linked. Therefore, the viral strategy to survive in vivo and transmit to new hosts is associated with its pathogenesis; adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases.

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