SARS-CoV-2 Infection: A Clinical and Histopathological Study in Pregnancy

Simple Summary SARS-CoV-2 infection is now known to be associated with several adverse events. However, not much is known about the effect it may have if contracted during pregnancy, on the proper development of the placenta or, subsequently, of the fetus itself. Studies have shown that there may be an increased incidence of developing pathological conditions, such as preterm delivery, fetal growth retardation, the onset of gestational diabetes or hypertensive disorders. In this study, several cases of women who became infected at different times during pregnancy (during the first, second or third trimester) were examined, and in particular it was assessed whether the infection had a role in altering the proper vascular development of the placenta. The greatest alterations were observed when infection occurred during the third trimester; alterations in the expression levels of certain markers of vasculogenesis such as the presence of fibrin deposits, lymphocyte infiltration in the villi, edema and thrombi were observed. Further studies are needed, however, as the mechanisms involved are not yet clear and therefore it is not yet possible to think of therapeutic strategies. During pregnancy, SARS-CoV-2 infection is associated with several adverse outcomes, including an increased risk of pre-eclampsia, preterm delivery, hypertensive disorders, gestational diabetes, and fetal growth restriction related to the development of placenta vascular abnormalities. We analyzed human placenta from full-term, uncomplicated pregnancies with SARS-CoV-2 infection during the first, second, or third trimesters of gestation. We studied, by the immunohistochemistry technique, the expression of CD34 and podoplanin (PDPN) as markers of vasculogenesis to find any differences. As secondary outcomes, we correlated maternal symptoms with placental histological alterations, including fibrin deposits, lymphocyte infiltration in the villi, edema, and thrombi. Our results showed a PDPN expression around the villous stroma as a plexiform network around the villous nucleus of fetal vessels; significant down-regulation was observed in the villous stroma of women infected during the third trimester. CD34 showed no changes in expression levels. During SARS-CoV-2 infection, the most common maternal symptoms were fever, anosmia, ageusia and asthenia, and the majority were treated with paracetamol, corticosteroids and azithromycin. Patients that required multiple symptomatic treatments evidenced a large amount of fibrin deposition in the villi. Certainly, PDPN plays a key role in healthy placental vasculogenesis and thus in its proper physiology, and SARS-CoV-2 surely alters its normal expression. Further studies are necessary to understand what mechanisms are being altered to try to avoid possible complications for both the mother and fetus in terms of the contagions that will still occur.