To expand our findings to earlier in human pregnancy, when the fetus is likely to face the more severe consequences of congenital T. gondii infections, we also utilized a midgestation chorionic villous explant model and show that second-trimester SYNs also resist T. gondii attachment and induce CCL22 in response to infection, whereas the fetus-derived amnion and chorion are permissive to infection and do not induce CCL22. The gene discussed is CCL22; the disease is infection.