Diverse infectious agents such as bacteria and viruses have been implicated by epidemiologic studies as likely environmental factors which may either predispose to or precipitate some cases of schizophrenia. For example, exposure to influenza in utero may increase the risk of developing schizophrenia later in life. Similarly, certain strains of influenza can directly precipitate a schizophreniform psychosis (e.g., the 1918 HINI pandemic strain). However, it is generally believed that influenza viruses do not infect the central nervous system in man, nor are they thought to reach the fetus, except in extremely rare circumstances. How can influenza predispose to or precipitate schizophrenia if it does not infect the brain itself? If schizophrenia is thought of not as a viral illness, but as an autoimmune disorder triggered by viruses, then these puzzling Facts can be reconciled. Thus, autoantibodies induced by influenza may cross the placenta las do antibodies to the acetylcholine receptor and the TSH-receptor) thereby causing subclinical brain damage which predisposes to schizophrenia. A similar mechanism could account for precipitation of schizophreniform psychosis by influenza. We have therefore tested twenty strains of influenza for their ability to induce anti-brain antibodies in rabbits, and find that certain H1N1 viruses induce autoantibodies to a 37kDa protein which is specific to brain where it is confined to gray matter. We have purified this protein to homogeneity and in collaboration with Dr. Brian Martin have obtained a partial amino acid sequence.
