Despite the nearly 100 million cases of Covid recorded to date worldwide, there is no strong evidence that the virus that causes the disease, SARS-CoV-2, poses a threat to fetuses.
This is confirmed by researchers from Duke University, in North Carolina, and the Mount Sinai School of Medicine in New York (United States), who have identified a mechanism in the placenta that could be the key to a viral infection from the mother during pregnancy does not harm the baby.
The mother’s immune response to fight the virus could harm the baby and the placenta does not allow it to penetrate, thanks to the estrogen receptors it contains.
An important advance to protect the baby if the mother is infected
When a person is infected by a virus, their immune system sends out a chemical signal called type I interferon, which signals surrounding cells to increase their antiviral defenses, including increased inflammation. This response helps prevent the virus from copying itself and gives the adaptive immune system more time to learn about the new invader and begin fighting it.
A pregnant woman who is infected with a virus generates these same defenses, but if these molecules crossed the placenta and reached the fetus, they would cause serious abnormalities in its development and even death. Of course, except in the case of a virus, such as Zika, it is normal that they do not replicate if they affect the fetus.
The study, published in Science Daily, has found a mechanism that protects the fetus from damage that could be caused by the mother’s immune response to a virus: they have identified a key player in this pathway, a cell-surface estrogen receptor called GPER1 that it is especially abundant in the placenta and fetal tissues.
Study leader Nicholas Heaton, associate professor of Molecular Genetics and Microbiology at Duke School of Medicine, notes that “this probably explains why many maternal infections during pregnancy do not harm the fetus.”
After a series of screenings, the researchers discovered that GPER1 receptors were concentrated in the placenta, where the mother’s blood supply transmits oxygen and nutrients to the fetus. Estrogen levels are much higher during pregnancy, making the GPER1 receptor even more capable of suppressing interferon signaling in the placenta and developing fetus.
Researchers still do not understand how this receptor protects, although they suspect that there are other mechanisms triggered by it, although they have found that:
“If we deactivate the GPER1 pathway, even normally benign maternal infections (like the flu) will now cause significant fetal development problems.”
Professor Heaton says that the good thing about this system being concentrated around the baby is that it protects the fetus from inflammation, while allowing the rest of the mother’s tissues to be better able to use interferon in the battle against it. virus.
Researchers will continue to study whether a possible “hyperactivation” of the GPER1 pathway would serve to protect the development of the baby in pregnancy when the mother is infected with the virus.
Via | Duke University School of Medicine
Photos | iStock
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