Human T cell leukemia virus type I (HTLV-I) has been linked to the development of an aggressive lymphoproliferative disorder (adult T cell leukemia), a chronic neurodegenerative presentation (HTLV-I-associated myelopathy/tropical spastic paraparesis) and numerous less well-defined inflammatory conditions. The viral regulatory protein Tax has been implicated in cellular transformation events leading to the onset of adult T cell leukemia. Details on the stepwise processes through which Tax induces morphological changes in cells are poorly understood. We show here that Tax can bind to a class of intermediate filaments, the cytokeratins (Kcr), Tax interacts with the 1 B helical coil of kcratin 8, a domain critical for higher-order intermediate filament matrix formation. Expression of Tax in epithelial cells visibly altered the structural pattern ofthe Ker network. In a T lymphocyte cell line, induction of Tax expression resulted in increased cellular adhcrence/invasion of Matrigel filters. We propose that one aspect ofTax function is the induction of morphological changes in cellular cytoskeletal structures. This finding for Tax-expressing cells might be one factor contributing directly to the pathogenesis of HTLV-1 disease(s).

Keywords:
HTLV-I, Cytokeratin, Invasive, Motility, HAM/TSP, Regulatory protein
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1997
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