This further implicates circulatory impairments in the disease pathology and provides the first evidence that placental responses to infection may not be in harmony with maternal responses, as maternal cells in the placenta showed elevated VEGF levels whereas fetal syncytiotrophoblasts produced more sVEGFR1, reducing VEGF bioavailability (Muehlenbachs et al., 2006). This evidence concerns the gene VEGFA and infection.