Abstract
Common features of patients with human T lymphotropic virus type I (HTLV-I) -associated myelopathy/tropical spastic paraparesis (HAM/TSP) compared to asymptomatic HTLV-I carriers include a genetically determined high cellular immune responsiveness to HTLV-I and a distributional bias of viral activation between the blood flow and central nervous system (CNS). It had been proposed that increased and altered in vitro late phase spontaneous proliferation (SP) of peripheral blood lymphocytes, which is concomitant with in vitro viral activation, is associated with the pathogenesis of HAM/TSP. To assess whether SP might epitomize the peculiar cellular inflammation in the CNS of patients with HAM/TSP, fractionated peripheral blood lymphocytes from HAM/TSP patients were employed to reconstitute this phenomenon in vitro. Although CD8+ cells had no inherent responsive potential in the absence of exogenous interleukin-2 (IL-2), the SP observed in CD4+ cell cultures was facilitated by the addition of autologous CD8+ cells to the cultures. It could be shown that proliferative responses of the CD8+ cells appeared against cultured and irradiated autologous CD4+cells but not against purified HTLV-I virions. These findings clearly demonstrate that the cellular response against the infected cells is involved and is one of the major components of the late phase SP, and support the view that this phenomenon may represent an in vitro counterpart of the susceptibility to HAM/TSP.
