Schizophrenia: genetics and the maternal immune response to viral infection.
Thirty years ago, Eliot Slater suggested that the reason schizophrenia was not progressively eliminated from the population was that the responsible gene also conveyed a compensatory advantage in terms of increased resistance to infection. If this selective advantage lies in the antibody response to certain viral infections, this could explain recent studies suggesting that exposure to influenza in the second trimester of gestation increases the risk of later schizophrenia. We propose that prenatal exposure to influenza induces maternal antibodies which then cross-react with proteins in the developing foetal brain, becoming foetal autoantibodies. Thus an immunogenetic response by the mother results in aberrant foetal neurodevelopment, the biological substrate for a proportion of adult schizophrenia. Initial research strategies to test this hypothesis are proposed.
Wright
P
P
Department of Psychological Medicine, Institute of Psychiatry, London, United Kingdom.
Gill
M
M
Murray
R M
RM
D000914:Antibodies, Viral / Q000096:biosynthesis*; D001323:Autoantibodies / Q000096:biosynthesis; D001921:Brain / Q000276:immunology; D005260:Female; D005333:Fetus / Q000276:immunology; D006680:HLA Antigens / Q000276:immunology; D006801:Humans; D007251:Influenza, Human / Q000150:complications / Q000276:immunology*; D008431:Maternal-Fetal Exchange; D009975:Orthomyxoviridae / Q000276:immunology*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology*; D011262:Pregnancy Trimester, Second; D012559:Schizophrenia / Q000209:etiology / Q000235:genetics* / Q000276:immunology
D000914:Antibodies, Viral; D001323:Autoantibodies; D006680:HLA Antigens