Teratogenic effects of the Zika virus and the role of the placenta

Abstract

The mechanism by which the Zika virus can cause fetal microcephaly is not known. Reports indicate that Zika is able to evade the normal immunoprotective responses of the placenta. Microcephaly has genetic causes, some associated with maternal exposures including radiation, tobacco smoke, alcohol, and viruses. Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly conveys the Zika virus to the early embryo or fetus. Alternatively, the placenta itself might be mounting a response to the exposure; this response might be contributing to or causing the brain defect. This distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies to prevent Zika-induced teratogenesis.

Figure:. The gestational sac in the first trimester before the onset of maternal–placental blood flow

The placenta consists of the chorion and the chorionic villi which encircle the embryo and carry out synthesis and secretion of molecules that can enter into the embryo. Different scenarios include: direct transfer of free virus through the trophoblast layers, placental exosome-mediated transfer, or minimal to no transfer.