HTLV-I infection is causally associated with a variety of human diseases including leukemia/lymphoma, myelopathy, uveitis, and arthropathy. Tax protein of HTLV-I, which is considered oncogenic, binds to transcription factors or other cytoplasmic cellular molecules involved in the fundamental cell function and thereby induces cellular changes. The interaction between HTLV-I–infected cells with dysregulated function and different kinds of cells in the host, such as lymphocytes and vascular endothelial cells through viral peptides, antigen receptors, cell adhesion molecules, and cytokines, appears to be one of the basic mechanisms underlying the development of HTLV-I–associated diseases. This interaction may play a major role in determining tumorigenicity and in forming clinical features of the diseases. The in vivo cell proliferation model of HTLV-I–infected cells using severe combined immunodeficient (SCID) mice can differentiate tumorigenicity from cell immortalization 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.


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  • Article Type: Review Article
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