HUMAN T-CELL LEUKEMIA-VIRUS TYPE-I (HTLV-I) AND HUMAN-DISEASES

HTLV-I infection is causally associated with a variety of human diseas es including leukemia/lymphoma, myelopathy, uveitis, and arthropathy. Tax protein of HTLV-I, which is considered oncogenic, binds to transcr iption factors or other cytoplasmic cellular molecules involved in the fundamental cell function and thereby induces cellular changes. The i nteraction between HTLV-I-infected cells with dysregulated function an d different kinds of cells in the host, such as lymphocytes and vascul ar endothelial cells through viral peptides, antigen receptors, cell a dhesion molecules, and cytokines, appears to be one of the basic mecha nisms underlying the development of HTLV-I-associated diseases. This i nteraction may play a major role in determining tumorigenicity and in forming clinical features of the diseases. The in vivo cell proliferat ion model of HTLV-I-infected cells using severe combined immunodeficie nt (SCID) mice can differentiate tumorigenicity from cell immortalizat ion in vitro. The OX40 and its ligand gp34, which are induced by HTLV- I infection and directly mediate the adhesion between HTLV-I-infected T cells and vascular endothelial cells, may be critically involved in the localization and proliferation of HTLV-I-infected cells in vivo.