Aim. Based on the analysis of literature data, to investigate the pathomorphological and ultrastructural changes in the placenta associated with COVID-19 during pregnancy, with the identification of critical periods for fetal development.

Materials and methods. A search for original research articles was conducted in the scientometric databases PubMed, Web of Science, Scopus, and Google Scholar published between 2017 and 2025. The following search terms were used: COVID-19, SARS-CoV-2, placenta, pregnancy, chorionic villi, and placental telocytes. A total of 44 publications were selected to summarize current knowledge on the issue.

Results. According to the literature, during the acute phase of COVID-19 in pregnant women, 100 % of cases showed placentitis, signs of endothelial dysfunction, damage to the microcirculatory bed, edema of the chorionic villi stroma, nuclear apoptosis, narrowing of the vascular lumen, and destructive changes in telocytes. As the post-COVID interval lengthened, manifestations of placentitis decreased and vascular lumens were restored (in cases of COVID-19 during the third trimester). In contrast, cases of infection in the second trimester were characterized by arteriolosclerosis, stromal fibrosis of the villi, and delayed chorionic maturation.

Conclusions. Vertical transmission of SARS-CoV-2 from infected pregnant women to their fetuses has been demonstrated, with no established correlation between the severity of maternal illness and the extent of placental or fetal impairment. The SARS-CoV-2 virus causes endothelial dysfunction, microcirculatory disturbances, edema, and placentitis, acting as a morphogenetic factor in chorionic remodeling. The degree of placental pathomorphological changes and the consequences for the fetus were determined by the gestational age at which maternal infection occurs. The loss of regulatory control by structurally damaged telocytes over angiogenesis, vascular tone regulation, and apoptosis constitutes one of the mechanisms underlying the development of placental insufficiency.