Introduction Maternal anti-SARS-CoV-2 Spike antibodies can cross the placenta during pregnancy, and neonates born to infected mothers have acquired antibodies at birth. Few studies reported data on the histopathological changes of the placenta during infection and placental infection. SARS-CoV-2 infection may cause impaired development of the placenta, thus predisposing maternal and fetal unfavorable outcomes. The prospective study aims to evaluate the risk of vertical transmission of SARS-CoV-2 and placental passage of anti-Spike antibodies as well as the impact of clinical severity on placental structures. Methods This is a prospective cohort study on 30 pregnant women infected by SARS-CoV-2 with their neonates. The demographic features and pregnancy outcomes were collected. Gross and microscopic examinations of the placentas were done. Maternal and umbilical cord sera were obtained at the time of delivery. Nasopharyngeal swabs were collected from neonates immediately after birth. Results The concentrations of total anti-SARS-CoV-2 Spike antibodies were higher in pregnant women with moderate to severe/critical disease. The maternal total anti-SARS-CoV-2 Spike levels were correlated with those of neonatal levels. The rate of placental abnormalities is high in the mothers with severe disease, and those with positive anti-SARS-CoV-2 IgM. All neonates had negative nasopharyngeal swabs for SARS- CoV-2 infections and all placentas were negative in immunohistochemical staining for Spike protein. Discussion The maternally derived anti-SARS-CoV-2 Spike antibody can transmit to neonates born to infected mothers regardless of gestational age. Our results indicated that the disease severity is associated with ischemic placental pathology which may result in adverse pregnancy outcomes.

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Background: The maintenance of vaginal microbiota is an important factor to achieve ideal pregnancy outcomes. Coronavirus disease has been shown to have potential adverse effects on pregnancy and neonatal outcomes. Pregnancy itself is a risk factor for the severity of COVID-19, with an increased risk of intensive care unit (ICU) admission, maternal morbidity, and mortality. the role of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in vaginal microbiome composition in pregnant women with COVID-19 has not yet been investigated. Therefore, we anticipate that COVID-19 may unfavorably affect the composition of the vaginal microbiota, resulting in adverse pregnancy outcomes. We aimed to describe the alterations of the composition of vaginal microbiota in pregnant women with COVID-19.Results: A prospective case-control study was conducted among 19 pregnant women with COVID-19 and 28 healthy controls matched according to the gestational week and age. The vaginal swabs were collected during the active phase of infection and consecutively, within a month after recovering from infection. In three patients, longitudinal samples before, in the course, and after infection were also obtained. The microbiome alterations were examined by 16S rRNA gene sequencing. We indicated that COVID-19 was associated with vaginal dysbiosis during pregnancy, which was indicated by an increased alpha diversity index. There was a signi cantly decrease in Firmicutes (P=0.007) and Lactobacillus (P=0.019) with an increase in Bacteroidetes (P=0.024) in the COVID-19 group. In the moderate/severe group, increased amounts of Ureaplasma and vanishing of Lactobacillus gasseri were found in women, compared to the asymptomatic or mild group (P=0.001). In longitudinal analysis, elevation of Actinobacteria with reduction of Firmicutes and Bacteroides were indicated during the active phase. Conclusions: The study revealed vaginal dysbiosis with a low abundance of Lactobacillus and an increase in Bacteroidetes in relation to SARS-CoV-2 infection. Vaginal dysbiosis in COVID-19 could be a contributing factor in pregnancy adverse outcomes. Trial registration: clinicaltrials, Registered 15

Introduction Preeclampsia is a pregnancy-associated disease in which hypertension, proteinuria, placental insufficiency, and fetal growth retardation occurs, and it is one of the leading diseases affecting both maternal and fetal mortality and morbidity (1,2). It is estimated that 7%-10% of all pregnancies are complicated with preeclampsia (3). Despite intense investigations, ethiopathogenesis of the disease is not clear yet (4). There are several findings of the disease such as abnormal placentation even detected in the early stages of the disease (5,6). Endothelial dysfunction causes increased responses to constrictor agents and reduced relaxations to acetylcholine and other related relaxing agents (7), aggravated inflammatory response (8), disruption in angiogenesis (4,9), and general vasospasm (10). It is shown that trophoblast invasion in the placenta is shallow in preeclampsia (11). From these findings, Redman et al. (3) proposed "two-stage model of preeclampsia". According to this hypothesis, interruption in trophoblast migration to Background/aim: Suramin is a potent angiogenesis inhibitor in rodents and attenuates placental development in rat pregnancy. We aimed to produce preeclampsia-like syndrome by suramin administration in rats and to investigate the functional responses in aortic, renal, and uterine arteries. Materials and methods: Pregnant and nonpregnant wistar rats received suramin (100 mg/kg, intraperitoneal) or equal volume of saline on days 10 and 11. Blood pressures of rats were observed daily. On the day 20, rats were executed. Protein levels in urine were measured and fetuses, placentas, and kidneys were weighted and evaluated. Thoracic aorta, renal, and uterine arteries were removed for functional studies. Results: Increased blood pressures and proteinuria were detected in suramin-given pregnant rats. Pathological examination of kidneys showed an acute tubular injury after suramin injection. Numbers and weights of fetuses and placentas were reduced in suramin-given pregnant rats. In functional studies, endothelial dysfunction occurred in uterine and renal arteries but not in the aorta. In this study, we showed that preeclampsia-like syndrome occurred in suramin-given rats. Conclusion: Our findings, which show that endothelial dysfunction occurred in uterine and renal arteries but not in the aorta, are consistent with the human findings of microvascular changes in preeclampsia.