title: A disturbance of interferon synthesis with the hyperproduction of unusual kinds of interferon can trigger autoimmune disease and play a pathogenetic role in AIDS: the removal of these interferons can be therapeutic.
abstract: Disturbances of interferon synthesis with the hyperproduction of unusual kinds of interferons may be the initial step which triggers autoimmune disease through a concatenation of pathological reactions including the disturbance of several immunological and interferon cascades. This fundamental disturbance can result either from a genetic predisposition or from the influence of certain viruses (or viral particles) or both factors together. The administration of interferons to individuals with an underlying or latent autoimmune condition can exacerbate or trigger the disease. AIDS has many features similar to autoimmune disease, including the hyperproduction of aberrant interferon, a type with little or no anti-HIV activity, protectively induced by HIV to allow its continued replication and survival. In other words, while most viruses induce normal IFN which protects the cells against viral infection, HIV induces an abnormal, defective kind of IFN which insures viral survival. The neutralization of hyperproduced interferons by polyclonal or monoclonal antibody produced in mouse, or preferably, human hybridoma, removal via extracorporeal means, or the use of antagonists which diminish the production or biological activity of these interferons can be a therapeutic approach to the management of these chronic diseases. In addition, the extracorporeal removal of different kinds of interferons, autoantibodies, autoantigens and other substances from the organism in certain pathological conditions may be an effective and safe method of treatment for autoimmune diseases and AIDS.
authors.affiliation: Advanced Biotherapy Concepts Labs, Rockville, MD.
authors.forename: S
authors.initials: S
authors.lastname: Skurkovich
authors.forename: B
authors.initials: B
authors.lastname: Skurkovich
authors.forename: J A
authors.initials: JA
authors.lastname: Bellanti
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology* / Q000503:physiopathology* / Q000628:therapy; D000818:Animals; D001327:Autoimmune Diseases / Q000503:physiopathology* / Q000628:therapy; D006681:HLA-D Antigens / Q000096:biosynthesis; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D006801:Humans; D007372:Interferons / Q000096:biosynthesis*; D008954:Models, Biological
chemical_list: D006681:HLA-D Antigens; D000949:Histocompatibility Antigens Class II; D007372:Interferons