Immunopathogenesis of HTLV-I associated neurologic disease: massive latent HTLV-I infection in bone marrow of HAM/TSP patients.

The localization of mammalian retroviruses to specified immune organs has significant implications on the pathophysiology of retroviral associated diseases. Human T-cell Lymphotropic Virus Type I (HTLV-I) is considered a CD4+ lymphotropic virus although the virus has been shown to infect a large variety of cells in vitro. Similarly, the human immunodeficiency virus (HIV), once thought to be harbored only in CD4+ peripheral blood lymphocytes (PBL) has been shown to be present in latent form in lymph nodes of HIV infected patients. HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) is a chronic progressive neurologic disorder of the central nervous system and is believed to result from infection of HTLV-I in association with an immunopathogenic or autoimmune mechanism. Here we describe experiments which utilize the in situ hybridization/polymerase chain reaction technology to demonstrate extensive HTLV-I infection of bone marrow in HAM/TSP patients. We discuss these results in the context of HTLV-I associated neurologic disease and extend these observations to other disorders of potential retroviral etiology and autoimmune involvement.