Abstract
As most recently demonstrated by the SARS-CoV-2 pandemic, congenital and perinatal infections are of significant concern to the pregnant population as compared to the general population. These outcomes can range from no apparent impact all the way to spontaneous abortion or fetal infection with long term developmental consequences. While some pathogens have developed mechanisms to cross the placenta and directly infect the fetus, other pathogens lead to an upregulation in maternal or placental inflammation that can indirectly cause harm. The placenta is a temporary, yet critical organ that serves multiple important functions during gestation including facilitation of fetal nutrition, oxygenation, and prevention of fetal infection in utero. Here, we review trophoblast cell immunology and the molecular mechanisms utilized to protect the fetus from infection. Lastly, we discuss consequences in the placenta when these protections fail and the histopathologic result following infection.
Highlights
Infections account for approximately 2 to 3% of all congenital anomalies [1]
Retinoic acid-inducible gene I (RIG-I), a cytoplasmic protein, is expressed in trophoblasts and can recognize both RNA and DNA viruses leading to a conformational change, oligomerization with mitochondrial antiviral signaling proteins (MAVS) and activates transcription of NF-kB [11,12,13]
Signaling though Toll-like receptors (TLR) and RIG-I leads to the production of type I interferons (IFN-α and IFN-β) which induce host anti-viral activity through the activation of both innate and adaptive immune responses
Summary
Infections account for approximately 2 to 3% of all congenital anomalies [1]. The placenta is a dynamic organ which is necessary for creating a protective barrier that keeps pathogens out. The complex interplay of the physiologic pathways within the placenta, it’s multifaceted role in both prevention of fetal rejection by the maternal immune system and protection from transmission of infections to the fetus is worth investigating, especially as risks of pandemics increase. Maternal immune responses that occur at the maternal-fetal interface are critical for the acquisition or protection from congenital or perinatal infections. The authors provide an overview of the cellular immunopathogenesis of the placental response towards invading infections. We discuss the molecular pathways involved and corresponding placental histopathologies with a specific focus on viral infections
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