Multiple Sclerosis: Clinical Trials with Interferons

Abstract

The rationale for the use of the interferons as treatment for multiple sclerosis (MS) is based upon a large body of evidence which documents a variety of immunological aberrations as well as various types of viral association in patients with this disease. Among the immunological abnormalities in MS are decreased numbers of suppressor T lymphocytes during exacerbations (1, 2), defective NK cell activity and defective in vitro interferon production (3). A possible viral etiology of MS has been proposed (4). Elevated serum and cerebrospinal fluid (CSF) levels of antibodies against viruses, particularly measles virus (5, 6), have been reported, as well as the isolation of a viral agent, termed the IM virus, from the CSF of several patients with MS (7, 8). Recently, evidence of a human T-lymphotropic virus type I (HTLV-I) type of virus has been found in patients with MS (9). A T-cell clone with some morphologic and histochemical properties of HTLV-I-infected cells has been established from an MS patient’s CSF. This clone grew independently of exogenous interleukin 2 (IL-2). It was postulated that this lymphotropic virus or its products play a role in the pathophysiology of MS by altering immune regulation (10).