Interferons are glycoproteins secreted in the body in response to viral infections and are presumed to provide protection to other cells against viral infection. The name derives from the term "viral interference" used in the first description of these proteins by their discoverers (Isaacs and Lindemann 1957). In addition to the antiviral properties, immunomodulatory and antineoplastic properties of interferons were discovered later (Borden and Ball 1981). Use of interferons in multiple sclerosis was based on the belief that the disease may be due to a latent virus infection of the brain in persons with impairment of the immune system (Cook and Dowling 1980). Trials with interferon have been conducted in various diseases of the nervous system including multiple sclerosis (Fleishman et al 1988). Two types of interferons have been identified: type 1 (interferon alpha and interferon beta) and type 2 (interferon gamma). Type 2 is synthesized mainly by lymphocytes and type 1 beta by fibroblasts, but both have a similar amino acid composition and genetic coding. Gamma interferon differs from type 1 interferons by its amino acid composition and cell surface receptor. Interferon alpha has been developed mostly for applications in virology and oncology. Interferon beta has a beneficial effect on the course of multiple sclerosis, and interferon alpha has an equivocal effect, whereas interferon gamma exacerbated the disease. Reasons for these varying effects are not well understood. History of development of interferon beta therapy for multiple sclerosis has been reviewed elsewhere (Stock and Horowski 2001).
Interferons are now manufactured commercially in large quantities by recombinant DNA technology. Interferon beta 1b was approved for the treatment of multiple sclerosis by the United States Food and Drug Administration in 1993, and the American Academy of Neurology issued guidelines for the management of patients receiving interferon beta 1b for multiple sclerosis (Lublin et al 1994).