Certain retroviruses of animal and human origin are im-munosuppressive, oncogenic, and neurotropic in their hosts. This pleiotropy is exemplified by the human T cell leukemia virus, type I (HTLV-I)[1]. Infection with HTLV-I is associated with an aggressive T cell malignancy, adult T cell leukemia (ATL)[2], a subacute or chronic leuke-mia that invariably terminates in a rapidly progressive malignant course, frequently associated with lymphadenopathy and hepatosplenomegaly, disseminated skin le-sions, and a proclivity toward invasion of the central ner-vous system, lungs, and gastrointestinal tract. More recently HTLV-I has been linked to a chronic, slowly progressive neurologic condition characterized by spastic paraparesis. Because case studies have emanated from clusters in tropical areas, including the Caribbean basin, India, and Africa, the term tropical spastic paraparesis (TSP) is commonly applied to this entity [3]. A similar condition described in Japan is referred to as HTLV-I-associated myelopathy (HAM)[4]. Two distinctly disparate clinical conditions, hematologic malignancy and neurologic spastic paraparesis, in association with the same or similar viral agent, raises many provocative questions concerning viral infectivity and host-immune responsiveness. By exploiting the differences between ATL and TSP one may hope to gain new insights into the underlying patho-genesis of both retrovirus-associated diseases. One particular biologic marker of the leukemic state is the elaboration of a clonally expanded population of hematopoietic cells. Clonality of T lymphocytes in ATL is reliably demonstrated by the presence of a dominant T cell receptor beta chain gene rearrangement [5] and by a pattern of clonal integration of HTLV-I proviral genome into host DNA [6]. Clearly, however, the demonstration of monoclonality is not restricted to cancer. For example, most cases of mono-clonal gammopathy fail to progress to myeloma [7] and monoclonal T cell proliferations are found in clinically benign lymphomatoid papulosis [8], the lymphoepithelial lesions in Sj6gren's syndrome [9], and in T gamma lymphoproliferative disease [10], a condition that may produce a limited lymphocytosis. In such patients the clonal