SARS-CoV-2, responsible for COVID-19, affects multiple bodily systems, including placenta. Understanding its effects on placental angioactive factors is vital due to its vascular implications. Herein, we hypothesized that maternal SARS-CoV-2 infection could impact placental morphology and the expression of angioactive and inflammatory factors. The study included 23 pregnant women tested for COVID-19 through reverse transcription polymerase chain reaction (RT-qPCR) and IgG serology around time of delivery and discriminated as: Viremia Group (VG, n = 6, maternal positive RT-qPCR, early infection), Serology Group (SG, n = 10, maternal positive serology, late infection), and Control Group (CG, n = 7, negative for SARS-CoV-2). PCR and immunolocalization of SARS-CoV-2 in the placenta tested negative. Placental morphology was examined using H&E-stained sections, along with immunostaining for vascular endothelial growth factor (VEGF), placental growth factor (PlGF), inducible and endothelial nitric oxide synthase (iNOS, eNOS), and cyclooxygenase 2 (COX2). SG showed a significant higher level of placental morphological changes compared to control samples, which included an increase in syncytial knots and fibrin deposits on the villous surface, and villous peripheral and central infarctions. In contrast, samples from VG exhibited more frequent vascular dilation, congestion, and chorioangiosis. Compared with the control group, immunohistochemical analysis showed significantly higher expression of VEGF (P = 0.001), COX2 (P = 0.03), and eNOS (P = 0.02) in VG. Conversely, in the SG, PlGF levels decreased (P = 0.01), while COX2 (P = 0.01) and iNOS (P = 0.01) levels were elevated. Our data suggests a temporal adaptation of the placenta to maternal SARS-CoV-2 infection, triggering structural, angioactive, and inflammatory responses, enhancing our understanding of potential placental pathways to cope with SARS-CoV-2 infection.
Quadros et al. (Tue,) studied this question.