From our past clinical observations, we have identified a cluster of cases with distinct neurological manifestations and, together with our viral studies, it has been proven that in fact these cases belong to a new clinical entity. The association of this slowly progressive spastic paraparesis with human T-cell lymphotropic virus type I (HTLV-I) enabled us to designate this clinical entity as HTLV-I-associated myelopathy or HAM. Later studies showed that 1) the geographical distribution of HAM follows that of adult T-cell leukemia (ATL) and 2) viruses detected in both disorders were identical by DNA blotting assay, but HAM and ATL are definitely expressed clinically as distinct from the other. In this regard, human leukocyte antigen (HLA) studies and the pattern of immune responsiveness seem to show a clear segregation of one from the other. As many initially studied cases have responded favorably to corticosteroids and had frequent perivascular cuffing in the spinal cord of a necropsied case, it is likely that, in part, immune events play a role in the pathogenesis. Our efforts are now directed to determining whether a) HAM is purely an autoimmune process, or b) a slow virus infection with a long incubation period may be the culprit.