25-Jan-2021 | Market Research Store
Researchers at Duke and Mt. Sinai have found a molecular pathway that helps stop a viral infection during the pregnancy from affected the baby inside the womb. It has been observed that when an individual is infected the immune system naturally releases chemical signals termed type I interferon which informs the adjacent cells about increasing their anti-viral defenses such as developing inflammation. The immune response helps avoid the virus from multiplying and thereby, gives the immune system some more time to learn about the foreign bodies before targeting them. In pregnant women, the same signals are to be generated in response to a viral attack but if these signal molecules and inflammation were to cross the placenta to reach the fetus, they are likely to cause extreme developmental abnormalities or even death.
There is no chance of the signal crossing the placenta except in case of the Zika virus and other virus that can replicate in the fetus and future harm it. The researchers have not got evidence that the SARS-CoV-2virus could pose any threat to fetuses. This is the reason the researchers found a new mechanism to protect the fetuses from being harmed through mother’s immune response to a viral infection. The researchers have been able to find a vital hero in this mechanism named cell-surface estrogen receptor called GPER1 that is present in abundance in the fetal tissues and placenta. It is the reason majority of the maternal infections do not harm the fetus.
On scrutinizing GPER1, this candidate was found in high amounts in the placenta from where the mother’s blood transports oxygen and nutrients to the fetus. Furthermore, the pregnant women have their estrogen levels surging which in turn give the GPER1 receptor more power to suppress interferon signaling in the placenta and growing fetus. On blocking the G15 compound and estrogen receptor the researchers saw slight abnormalities in the mouse pups. They also found the addition of G15 to cause fetal defects. The researchers are thus still mind boggled over how GPER1 provides this protection. They guessed that the receptor activates downstream mechanisms. However, the surprising part of this system is that its concentration around the fetus protects unborn baby from inflammation while permitting the rest of mother’s tissue to use interferon to combat the virus. The next study is to test if hyperactivation of the GPER1 pathway would protect fetal development when a mother is virally infected.