ABSTRACT
Page 5452. In the "2.1. Preparation of CCM-CDs" section in the Experimental Section, "Curcumin (CCM;0.30 g) and citric acid (0.60 g) were ground uniformly, sealed, and hydrothermally treated in a 25 mL Teflon-lined autoclave at 180 C for 1 h." was incorrectly written. It should be "Curcumin (CCM;0.30 g) and citric acid (0.60 g) were ground uniformly, sealed, and hydrothermally treated in a 25 mL Teflon-lined autoclave at 180 C for 1.5 h.". This change does not affect the conclusion of this paper. Page 5455. In the caption of Figure 6c, "Virus titers calculated in the presence and absence of EDA-CDs or CCMCDs. The pictures were taken at 12 hpi." was incorrectly written. It should be "Virus titers calculated in the presence and absence of EDA-CDs or CCM-CDs. The pictures were taken at 9 hpi.". In addition, the fluorescence images of the DAPI and Merge in the EDA-CDs (125 g/mL) group (Figure 6a) were chosen by mistake when the artwork was submitted. These changes do not affect the conclusion of this paper. The revised Figure 6a, which now shows the correct images from the original data source, is as follows: (Figure Present). © 2022 American Chemical Society. All rights reserved.
ABSTRACT
Background: The rarity of placental infection by SARSCoV- 2 suggests the presence of protective measures. SARS-CoV-2 requires coexporession of its receptor, ACE2, and the serine proteinase TMPRSS2 for cellular infection. Both are expressed in the placenta but their protein expression pattern has not been demonstrated to date. Methods: 19 placentas from women with PCR proven SARS-CoV-2 infection were examined for SARS-CoV-2 expression by RNAish and immunohistochemistry (IHC) and for ACE2 and TMPRSS2 by IHC. Gross and histopathology were also reviewed. Two sets of controls were used: 'normal controls' - 122 placentas examined solely for GBS exposure (no other indication for examination) delivered from 2000-2004;and 'abnormal controls' - 130 placentas from neonates with a clinical diagnosis of HIE delivered from 2000-2019. The control placentas were reviewed for gross and histopathology. Results: 2 cases showed placental infection with viral RNA the villous syncytiotrophoblast (ST) and cytotrophoblast (CT) in a patchy distribution in 1 and only focally in the other. The infant with the patchy infection was SARSCoV- 2 PCR positive at 24 hours, the infant with only focal infection was PCR negative. None of the other placentas showed viral infection. All placentas showed robust expression of ACE2 in the trophoblast. The ST and CTexpression was membranous and In most cases ST expression was polarized-strongest, and in many cases only present, on the villous stromal side of the ST. TMPRSS2 was weakly expressed in the placental endothelial cells. Hofbauer cells were negative for both. We did not find a an increase in maternal or fetal vascular malperfusion (MVM or FVM) over controls. We saw MVM at 25%, FVM at 20%, acute chorioamnionitis at 30%, inflammatory pathologies (1 case each of ungradable VUE, intervillositis, Hofbauer cell hyperplasia) at 15%, all within published prevalences and similar to our controls. Conclusion:We did not find increased prevalence of MFM, FVM, infectious, or inflammatory pathology above published our our sets of controls as other have, perhaps due to small sample size. SARS-CoV-2 infection of the placenta is rare and vertical transmission, if it occurs, is even rarer. One mechanism for this is the rare occurrence of maternal SARS-CoV-2 viremia. Another mechanisms might be the unfavorable expression ACE2 and TMPRSS2. We show that their expression is uniquely distinct: ACE2 in the tropohobast and TMPRSS2 in the endothelium. Although we did not detect coexpression we cannot rule out that the vascular-syncytial membranes might coexpress ACE2 and TMPRSS2. We also show that ACE2 expression is polarized in most cases away from the maternal vascular space thereby perhaps limiting SARS-CoV-2 access to ST infection.