The placenta is a temporary organ that develops during pregnancy, serving as a lifeline between the pregnant individual and the developing fetus. It performs functions fundamental for healthy fetal growth and development. Understanding the typical characteristics of a healthy placenta provides a basis for recognizing changes observed when a pregnancy is affected by maternal COVID-19 infection. This article explores the differences between a normal placenta and one impacted by maternal SARS-CoV-2 infection, drawing on scientific findings.
The Placenta’s Functions in a Normal Pregnancy
The placenta performs multiple roles, acting as the baby’s temporary lungs, kidneys, and liver throughout gestation. It facilitates the exchange of nutrients and oxygen, transferring essential substances like glucose, amino acids, fatty acids, and vitamins from the maternal bloodstream to the fetus, alongside oxygen crucial for fetal respiration. This exchange occurs without direct mixing of maternal and fetal blood, separated by a thin barrier.
The placenta is also responsible for waste removal from the fetal circulation. It filters metabolic waste products, such as carbon dioxide, back into the mother’s system for excretion. This maintains a healthy internal environment for the growing fetus.
The placenta also functions as an endocrine organ, producing various hormones that regulate both maternal and fetal physiology. Hormones like human chorionic gonadotropin (hCG) help to maintain the pregnancy by supporting the uterine lining. Progesterone prevents uterine contractions and supports growth. Human placental lactogen (hPL) is also produced, playing a role in fetal metabolism and growth.
Inflammation and Immune Response in the COVID-Affected Placenta
Placentas from pregnancies affected by maternal COVID-19 infection often exhibit a strong immune reaction. A common finding is intervillositis, characterized by an infiltration of maternal immune cells, including macrophages and T-lymphocytes, into the intervillous space [S2-1, S2-2, S2-3, S2-4, S2-5].
Chronic Histiocytic Intervillositis (CHI) is a specific pattern of inflammation frequently observed. This condition is marked by significant collections of histiocytes, a type of macrophage, within the intervillous spaces, often accompanied by necrosis of the syncytiotrophoblast, the outer layer of placental villi interfacing with maternal blood [S2-1, S2-2, S2-3, S2-5]. In some instances, the virus itself has been directly detected within the syncytiotrophoblast, supporting the idea that the inflammation is related to the viral infection [S2-1, S2-2, S2-3, S2-4].
The SARS-CoV-2 virus utilizes the Angiotensin-Converting Enzyme 2 (ACE2) receptor for entry into human cells, and these receptors are present in placental tissue [S2-1, S2-3, S2-4]. Studies indicate that ACE2 expression in the placenta can be upregulated under hypoxic (low oxygen) conditions, potentially increasing placental susceptibility to viral infection and inflammation [S2-1]. Viral components, such as SARS-CoV-2 nucleocapsid protein and genomic RNA, have been identified primarily in the syncytiotrophoblast layer, highlighting this layer as a target for infection [S2-1, S2-2, S2-3, S2-4].
Impaired Blood Flow and Tissue Damage
Beyond the inflammatory changes, placentas from individuals with COVID-19 frequently show physical and vascular consequences affecting blood circulation. Maternal Vascular Malperfusion (MVM) is a common finding, indicating issues with blood flow originating from the mother’s side of the placenta [S3-1, S3-2, S3-3, S3-4, S3-5]. This can manifest as narrowed or damaged maternal arteries, or an increased presence of syncytial knots, which are clusters of syncytiotrophoblast nuclei that can be a sign of placental stress [S3-3, S3-5].
Increased thrombosis, or blood clot formation, is also observed within placental vessels [S3-1, S3-2, S3-3, S3-5]. These clots can occur in both maternal and fetal placental vessels, physically obstructing or slowing blood flow [S3-2]. Fetal vascular thrombosis is a frequently documented feature in COVID-affected placentas [S3-5].
Excessive fibrin deposition, an accumulation of a protein involved in blood clotting, is another common finding [S3-1, S3-2, S3-3, S3-4, S3-5]. This fibrin can build up in the intervillous space, where nutrient and oxygen exchange takes place, creating a physical barrier that impedes essential substance transfer to the fetus [S3-1, S3-3]. This deposition is often seen in conjunction with chronic histiocytic intervillositis and trophoblast necrosis, suggesting a complex interplay of inflammatory and vascular damage [S3-1, S3-3, S3-4]. Other observed changes include villous infarcts and avascular villi, which are areas of placental tissue damaged by insufficient blood supply [S3-1, S3-2, S3-3].
Potential Effects on Fetal Development and Health
Placental damage in pregnancies affected by COVID-19 can have consequences for fetal development and overall health. Impaired nutrient and oxygen flow, resulting from the discussed placental pathologies, can lead to Fetal Growth Restriction (FGR), also known as intrauterine growth restriction (IUGR) [S4-1, S4-2, S4-4, S4-5]. This means the baby may not grow at the expected rate due to the placenta’s reduced ability to supply necessary resources [S4-2, S4-4].
A poorly functioning placenta, often experiencing reduced oxygen delivery (hypoxia), can result in fetal distress. This can manifest as signs of compromise during pregnancy or labor [S4-1, S4-5].
In severe cases of placental damage, an increased risk of stillbirth (intrauterine fetal demise) has been reported with maternal COVID-19 infection [S4-1, S4-2, S4-3, S4-5]. This rare outcome highlights the potential severity of placental pathology linked to the virus [S4-2].
There is also an association between placental issues in COVID-affected pregnancies and an increased likelihood of preterm birth [S4-1, S4-2, S4-3, S4-4, S4-5]. Pregnant individuals with symptomatic SARS-CoV-2 infection have shown a greater propensity for preterm labor, highlighting the impact of the infection on the timing of delivery [S4-5].