Prenatal viral infection has been called the principal non-genetic cause of autism. Prenatal exposure to rubella or cytomegalovirus activates the mother’s immune response and greatly increases the risk for autism. Congenital rubella syndrome is the most convincing environmental cause. Infection-associated immunological events in early pregnancy may affect neural development more than infections in late pregnancy, not only for autism but also for other psychiatric disorders of presumed neurodevelopmental origin, notably schizophrenia.
The maternal antibody theory hypothesizes that immunoglobulin G (IgG) in a mother’s blood can cross the placenta, enter into the fetus’s brain, react against fetal brain proteins, and cause autism. The theory is related to the autoimmune disease hypothesis, except it focuses on maternal antibodies rather than the child’s.
A 2008 study found that these antibodies bind to fetal brain cells, most commonly in mothers of children with regressive autism.
A 2008 study found that rhesus monkeys exposed during gestation to IgG from mothers of children with ASD demonstrated stereotypies, one of the three main symptoms of autism.