16:25-16:45 COVID-19 and intriguing placental data

• Published in: Journal of reproductive immunology Vol. 158; p. 103552
• Main Authors: Tallarek, Ann-Christin, Urbschat, Christopher, Brito, Luis Fonseca, Stanelle-Bertram, Stephanie, Krasemann, Susanne, Frascaroli, Giada, Thiele, Kristin, Wieczorek, Agnes, Lütgehetmann, Marc, Markert, Udo R., Hecher, Kurt, Brune, Wolfram, Stahl, Felix, Gabriel, Gülsah, Diemert, Anke, Arck, Petra Clara
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01-08-2023
• ISSN: 0165-0378; 1872-7603
• DOI: 10.1016/j.jri.2022.103552

The placenta is the fetal-maternal interface that supplies the fetus with nutrients, oxygen and immunoprot ective factors but also exposes it to exogenous noxae. Several viral pathogens like cytomegaly, rubella and Zika virus are known to be able to pass the transplacental barrier with far-reaching consequences such as miscarriage, stillbirth, malformations or severe fetal infection. Logically the emergence of the SARS-CoV-2 pandemic was associated with the concern of a possible vertical transmission which seemed to be confirmed in the first case reports. Fortunately over time large cohort studies and meta-analyses could show that vertical transmission with direct fetal infection of the fetal organs is rare complicating only 1-3% of SARS-CoV-2 infections in pregnancy
We will present our own data confirming and explaining why vertical transmission of SARS-CoV-2 with direct fetal infection seems to occur only in a minority of cases.
Our comprehensive placental analyses were able to identify a paucity of SARS-CoV-2 viral expression ex vivo in term placentae under acute infection and in convalescent pregnant women. Furthermore we could show inefficient SARS-CoV-2 replication in placental tissues in vitro, which provides a rationale for the low ex vivo viral expression. We detected specific SARS-CoV-2 T cell responses in mothers within a few days upon infection, which is undetectable in cord blood.
Nevertheless current studies show a significantly elevated risk for perinatal mortality including stillbirth. There is growing evidence that the major cause of perinatal deaths among fetuses and neonates having placentas compromised by SARS-CoV-2 is due to placental insufficiency. SARS-CoV-2 placentitis is defined by increased perivillous fibrin deposition, histiocytic intervillositis and trophoblast necrosis. These changes can cause extensive placental damage leading to placental malperfusion and insufficiency that is incompatible with intrauterine survival. This locally confined changes of the placenta need our further vigilance and evaluation.