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 chain of pathological reactions including the disturbances of several immunological and cytokine cascades. Prolonged circulation of this interferon may be a predictive marker of an autoimmune condition; the administration of interferons to animals or humans with autoimmune disease or an underlying or latent autoimmune condition can exacerbate or trigger the disease. Healthy people do not have interferon in their blood. This fundamental disturbance of interferon synthesis can result either from a genetic predisposition or from the influence of certain viruses (or viral particles) or both factors together. AIDS has many features similar to autoimmune disease, including the hyperproduction of aberrant interferon, a type with restricted anti-HIV activity, protectively induced by HIV to allow its continued replication and survival. This interferon stimulates the production of certain cytokines and autoantibodies which help unleash the potentially self-destructive powers of the immune system, bringing immunological chaos. In other words, while usual viruses induce normal interferon, which protects the cells against viral infection, HIV induces an abnormal, defective kind of interferon which ensures virus survival. Since there is no known effective method of destroying HIV directly, removing links in this chain of reactions could indirectly destroy HIV and possibly help restore immune functioning.(ABSTRACT TRUNCATED AT 250 WORDS)
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 / Q000209:etiology* / Q000378:metabolism / Q000628:therapy; D000818:Animals; D001327:Autoimmune Diseases / Q000378:metabolism*; D006681:HLA-D Antigens / Q000096:biosynthesis; D006801:Humans; D007372:Interferons / Q000096:biosynthesis*
chemical_list: D006681:HLA-D Antigens; D007372:Interferons