Funding outcome

The placenta is a fetally-derived organ that develops during pregnancy to support the developing fetus. Only a handful of viruses can infect the placenta. Much of the placenta's resistance to infection is due to a cell known as the syncytiotrophoblast (ST). The ST spans the maternal facing surface of the placenta as one giant cell. As a single cell, there are no gaps in the ST, helping defend against viruses that would normally try to squeeze between cells. One of the few viruses that can infect the placenta is Zika virus which is transferred by mosquitos. Currently there is no vaccine for Zika virus and infection often goes unnoticed. When infection occurs in the first three months of pregnancy, it can cause congenital Zika syndrome, characterized by a significantly smaller head of the child--a condition known as microcephaly. It is known that placental inflammation contributes to the development of congenital Zika syndrome. Dying cells can cause inflammation and our lab has discovered that Zika virus causes ST cell death, contributing to placental inflammation. This project aims to identify how Zika virus causes ST death by identifying which receptors the virus interacts with in this important cell type. We will test our hypothesis with human placental tissue and cultures to identify which receptors are expressed and if we can interfere with them to reduce cell death. Knowing how Zika virus is recognized by the placenta and leads to ST cell death can provide insight into potential treatments for congenital Zika syndrome.