Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during pregnancy appears to be associated with a higher incidence of hypoxia and placental dysfunction as indicated by the upregulation of genes associated with vasodilation, oxidative stress and preeclampsia (Stylianou et al. 2024), a condition referred to as a preeclampsia-like syndrome, occurring during severe COVID-19 (Leavitt et al. 2021; Naeh et al. 2022). Previously, Mittelberger and colleagues (2023) reported the downregulation of programmed cell death protein 1 and the programmed cell death ligand 1 (PD-L1) on macrophages and Hofbauer cells in the placenta of patients with PE. In the present study, the same group (Seefried et al. 2025) analyzed the expression of PD-L1, as well as CD68 and CD163, in the placenta from patients suffering from acute COVID-19 infection, and survivors of COVID-19 (post-COVID-19), as compared to healthy subjects. Central parts of the placenta, from ten female and male offspring from each of the three study groups, containing decidua and extravillous, as well as villus trophoblasts were investigated, and the numbers of antigen-presenting macrophages, Hofbauer cells, and extravillous trophoblast cells were calculated. The intensity of PD-L1, as well as of CD68 and CD163 as detected by immunohistochemistry, was quantified using a semiquantitative percentage core. In addition, double immunofluorescence was applied to typify the PD-L1-positive cells. The results of this meticulous and well illustrated investigation can be summarized as follows: PD-L1 immunostaining in the decidual stroma was significantly increased in male but not in female offspring placentas of women suffering from acute COVID-19, and enhanced in male offspring placenta post-COVID-19. The PD-L1 immunoreactive cells in the male offspring decidua of patients with acute COVID-19 were at least in part CD163-positive macrophages; however, in post-COVID-19 male offspring placentas there were CD163-positive macrophages, and additionally, extravillous trophoblast cells, both in close vicinity. In conclusion, the observed COVID-19-related changes in placental PD-L1 expression were gender related, as they were observed in male, but not in female, offspring. Rightfully, the authors propose to analyze the possible imprinting effects on the male COVID-19 offspring.