Virus doubles risk of having autistic child: study
Pregnant woman’s immune response to genital herpes can affect fetus
Women who become infected with genital herpes during early pregnancy, or experience a flare-up of the sexually transmitted disease, have twice the risk of giving birth to a child later diagnosed with autism, according to a new longitudinal study published Wednesday.
The study, led by the Center for Infection and Immunity at Columbia University, is the first to make the link between a pregnant woman’s immune response to a virus and the risk of her offspring developing autism spectrum disorder (ASD).
“We believe the mother’s i mmune response to HSV-2 (genital herpes) could be disrupting fetal central nervous system development, raising risk for autism,” says lead author Milada Mahic, a postdoctoral research scientist with the centre and also the Norwegian Institute of Public Health.
Published in mSphere, a journal of the American Society for Microbiology, the study sheds light on ASD, a group of complex neurological disorders characterized by difficulties with communication, social challenges and a tendency to repeat specific behaviours. About one in 68 diagnosed children is on the autism spectrum, according to Autism Speaks Canada.
“The cause, or causes, of most cases of autism are unknown,” says senior author Dr. Ian Lipkin, who’s also director of the centre. “But evidence suggests a role for both genetic and environmental factors. Our work suggests that inflammation and immune activation may contribute to risk. Herpes simplex virus-2 could be one of any number of infectious agents involved.”
In Canada, about 16 per cent of females aged 14 to 59 have genital herpes, according to Statistics Canada. For some, the lifelong infection can cause painful sores on the genital area, while others have no symptoms or visible sores. After sores from the first attack heal, the virus goes into a dormant stage, but recurrent outbreaks can occur, according to Health Canada.
The study’s authors looked at blood samples from 412 mothers of children diagnosed with ASD and 463 mothers of children without ASD who are enrolled in the Autism Birth Cohort (ABC) Study conducted by the Norwegian Institute of Public Health. (The study is part of the larger Norwegian Mother and Child Cohort Study, in which some 90,000 pregnant women were recruited between 1998 and 2008 to help with the study of disease.)
They studied samples taken around 18 weeks of pregnancy and at birth, looking for a link between maternal infection and the risk for ASD. They focused on a group of in- fectious agents that can cause miscarriage and birth defects, known collectively as TORCH: Toxoplasma gondii, Rubella, Cytomegalovirus and Herpes Simplex viruses type 1 (HSV-1 or oral herpes) and type 2 (HSV-2 or genital herpes).
They looked at the levels of antibodies to each of the TORCH pathogens and found high levels of HSV-2 antibodies correlated with increased risk for ASD in boys. (There were too few females with ASD for researchers to conclude if the effect is sex-specific.) This link was only evident in the blood samples taken during mid-pregnancy. Because it takes weeks for the body to make large amounts of antibodies, infection — or reactivation of infection — occurred during early pregnancy, when the fetal nervous system is undergoing rapid development.
The study’s authors suggest that placental inflammation, exposure of the fetus to inflammatory molecules produced by the placenta, or the transfer of maternally produced antibodies across the placenta, can cause fetal brain inflammation and increase the risk for ASD.
“There’s no evidence that this virus is actually going in to infect the fetus,” says Lipkin, adding such transmissions are rare and typically result in fetal death in utero.
“The important factor here is not the virus itself, but the immune response to the virus that is causing the damage.
“What we’re really doing is proposing a model that we think is going to be generic for understanding how these things might occur. And it likely has implications for a wide range of other sorts of systemic disorders.”
The longitudinal study is the first to make the link between a pregnant woman’s immune response to a virus and the risk of her offspring developing the disorder.
Dr. Ian Lipkin, above, says it’s not the virus itself, but the mother’s immune response to it that raises the risk for autism in the fetus.