CMV is the primary viral cause of congenital disease. If a mother is infected with CMV during pregnancy, the virus can pass to the fetus and cause congenital CMV. Symptoms include vision problems, an enlarged liver or spleen, small head size, and nervous system problems.

Here's some information about how cytomegalovirus (CMV) and FcRn interact in the placenta:

CMV replication
CMV replication proteins can be found in villus cytotrophoblasts in placentas with low to moderate CMV-neutralizing antibody titers. This suggests that the virus is transcytosed across the surface.

CMV-specific IgG
In placentas with high CMV-neutralizing antibody titers, syncytiotrophoblasts contain viral DNA and vesicles that contain both IgG and CMV glycoprotein B.

FcRn inhibition
Human cytomegalovirus (HCMV) can use US11 to inhibit FcRn functions. US11 blocks FcRn trafficking to the endosome, which reduces IgG transcytosis across the placenta.

FcRn expression
FcRn expression increases during pregnancy, especially in the third trimester. This means that antibody transfer is reduced in early gestation.