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New Research Explores a Mechanism by which CMV May Disrupt Fetal Development

By March 31, 2015Cytomegalovirus ("CMV")

New research led by Dr. Lenore Pereira, Ph.D., and supported in part by grants from the National Institute of Health, provides insights into the underlying mechanism by which congenital cytomegalovirus (“CMV”) infection may impact fetal development.

Dr. Pereira’s research highlights the importance of the placenta in the maintenance of a healthy pregnancy. Previous research has shown that infection of the placenta by CMV may deprive the fetus of oxygen and other nutrients, limiting fetal growth and, in severe cases, causing death. Thus, viral infection of the placenta, even in the absence of fetal infection, could be an important contributor to birth defects.

The placenta serves as the interface between the mother and fetus, allowing for nutrient uptake, gas exchange, and waste elimination. Dr. Pereira believes that CMV may interfere with the development and functioning of the placenta, which in some cases may restrict the transport of substances from maternal blood and contribute to the poor growth of a fetus during pregnancy.

Dr. Pereira and her team found evidence that CMV interferes with the development of trophoblast progenitor cells (“TBPCs”), a type of stem cell that gives rise to the mature cells of the chorionic villi.

The chorion is a membrane that connects the fetus to the uterus, providing both protection and nutrition. Chorionic villi sprout from the chorion in order to give a maximum area of contact with maternal blood. In the chorion of healthy pregnant women, TBPC’s will mature into syncytiotrophoblasts, found on the surface of the floating villi, and invasive cytotrophoblasts, cells that help route blood flow through the placenta for the growing fetus to use.

In vitro studies performed by Dr. Pereira revealed that CMV replicates in TBPC lines cultured from the chorionic membranes of pregnant women. This research indicates that CMV replication may disrupt the normal process by which TBPCs self-renew and mature into syncytiotrophoblasts and cytotrophoblasts. As a result, the placenta may suffer development defects that reduce its ability to transport nourishing substances from maternal blood to the fetus.

This study provides insight into the mechanism by which CMV may impair placental development, helping to explain a possible source of developmental defects associated with congenital CMV infection.

Dr. Pereira’s work may also provide insight into potential treatment strategies. In vitro studies performed by her team showed that a human monoclonal antibody to CMV glycoprotein B (gB) may restore the ability of TBPCs to self-renew and differentiate. Thus, TBPCs may have potential utility in the development of antiviral antibodies that could one day protect or restore healthy placental development and function.