Study Connects Maternal Response to Infection During Pregnancy with Increased Autism Risk

Feb. 22, 2017

Washington, DC – February 22, 2017 – A new study adds to a growing body of research aimed at understanding how a mother’s body’s response to infection influences a growing fetus. In research published this week in mSphere, researchers at Columbia University report that the sons of pregnant women who tested positive for antibodies against genital herpes (herpes simplex type 2, or HSV-2) at mid-pregnancy are more likely to be diagnosed with an autism spectrum disorder. The study is the first to connect maternal response to infection with autism risk. 

Genital herpes is a sexually-transmitted and contagious lifelong infection. The virus often remains inactive with occasional flare-ups. Importantly, the researchers did not conclude that a mother's herpes infection causes autism, or that the virus reaches the fetus. “If herpes were to cross the placenta and get to the fetus, it would most certainly die,” says W. Ian Lipkin, senior author on the study and director of Columbia University's Center for Infection and Immunity. 

Rather, the researchers suspect that the herpes infection triggers a cascade of chemicals in the mother's body, some of which may cross the placental barrier. 

“We believe the mother’s immune response to HSV-2 could be disrupting fetal central nervous system development, raising risk for autism,” says lead author Milada Mahic, at Columbia University’s Center for Infection and Immunity and the Norwegian Institute of Public Health.

The researchers analyzed blood samples collected at two times — at 18 weeks of pregnancy and at birth — from 442 mothers of children diagnosed with autism spectrum disorders and 464 mothers of children who didn’t have autism. They concentrated on five pathogens associated with birth defects and miscarriage: Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex viruses type 1 and 2.

Among those agents, only antibodies to herpes simplex virus type 2 correlated with a rise in autism rates — and only for boys. (They found no significant association in daughters.) Boys born to mothers with such antibodies against herpes simplex virus type 2 had double the risk of being diagnosed with autism.  

“That is a substantial increase in risk,” says Lipkin. The Centers for Disease Control and Prevention estimates that about 1 in 45 children have autism — roughly the same proportion as the number of children with Down Syndrome born to women in their early 40s.   

The cause or causes of autism spectrum disorders have eluded researchers, but both genetic and environmental factors may be important. The new study suggests that maternal infection with herpes may be a risk factors for autism in a child, especially if future studies can replicate these findings.  

The new research is consistent with previous animal studies showing that exposure to immunological mediators — like some cytokines — during fetal development can lead to neurodevelopmental conditions analogous to autism. Earlier epidemiological studies have also found connections between maternal immune responses and long-term developmental and behavioral problems in children.  

Lipkin thinks that ultimately, many neurodevelopmental problems will be linked to maternal immunological responses. Right now, he’s studying the effects of the influenza virus.

 “I think it’s going to be increasingly important to look at ways in which women become exposed to infectious agents during pregnancy,” he says, “and find ways we can modify the immune response to minimize the risk to the fetus.” 

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