Protecting fetuses from dangerous diseases has long been a concern for expecting mothers. Often, a pregnant woman will do all in her power to ensure her own health while her fetus is developing. Her body also works toward this goal with the development of the placenta. The placenta shields the fetus from the spread of disease — including viruses — between mother and fetus by providing a physical barrier interfacing the maternal and fetal blood systems. But how exactly is a fetus protected from a viral infection?

A new study has found that cells in the placenta, called trophoblasts, are scattered throughout the placenta and limit the spread of dangerous viruses. Viruses can easily spread from mother to child by going through the placenta. Viral infection during these early stages of growth and development can cause fetuses to have neurodevelopmental disorders or birth defects, and they may even die in the womb as a result of viral infection.

In the study, researchers found that primary human trophoblast (PHT) cells were resistant to a wide range of viruses like herpes simplex 1, poliovirus, and cytomegalovirus. The PHT cells were found to block the binding of viruses to them altogether, and so they could not be infected. As a result of their survival, the PHT cells send signals to other cells in the placenta so that they too can become resistant to infection by the virus. The signals can also cause infected cells to die quickly and prevent the spread of the virus.

The signals sent by PHT cells are significant, as they differ from traditional signals sent between cells. The signals are made up of short pieces of microRNA. MircoRNA is a small piece of genetic information that works mainly by binding to longer units of genetic information to block, or turn off, the cell it is in from using that piece of information. If genetic information is blocked from use, a number of changes can occur — especially to the cells themselves. In the case where it causes cells to defend themselves from viral infection, the microRNA is likely turning off the cell's capability to be negatively affected by the virus, or even altering the surface of the cell so the virus does not recognize it as a target to infect. This mechanism protects the fetus from infection because the layer of tissue blocking it from its mother's circulatory system is working to keep agents from leaving the mother and entering the fetus.

As a result, the virus cannot get past the placenta to infect the fetus. By no means is this an immune reaction. Neither the fetus nor the mother is immune to the virus after PHT cells cause the placenta to become impervious to the virus's passing. Instead, the mother is still infected by the virus, but the fetus is physically protected from exposure to the virus because of the placenta's action against the virus itself.

Similarly, this mechanism of action only works while a fetus is on the other side of a placenta. The researchers found that the PHT cells stop signaling in the first 24 hours after birth. This suggests that the placenta relies on both mother and child to operate appropriately.

While pregnant women should still be careful about their health, in order to ensure their child's health, it is reassuring to know that there are natural mechanisms in place to protect fetuses from being harmed while in the womb. "Our results suggest this pathway could be a powerful evolutionary adaptation to protect the fetus and mother from viral invaders," said Carolyn Coyne, Ph.D., co-senior investigator of the study. "We might be able to use these microRNAs to reduce the risk of viral infection in other cells outside of pregnancy, or perhaps to treat diseases where enhancing autophagy would be beneficial."

Source: Delorme-Axford E, Donker RB, Mouillet JF, et al. Human placental trophoblasts confer viral resistance to recipient cells. PNAS. 2013.

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