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Placental Pathology of COVID-19 with and without Fetal and Neonatal Infection: Trophoblast Necrosis and Chronic Histiocytic Intervillositis as Risk Factors for Transplacental Transmission of SARS-CoV-2
Viruses ( IF 5.818 ) Pub Date : 2020-11-15 , DOI: 10.3390/v12111308
David A. Schwartz , Denise Morotti

The mechanism(s) by which neonates testing positive for coronavirus disease 2019 (COVID-19) acquire their infection has been largely unknown. Transmission of the etiological agent, SARS-CoV-2, from mother to infant has been suspected but has been difficult to confirm. This communication summarizes the spectrum of pathology findings from pregnant women with COVID-19 based upon the infection status of their infants and addresses the potential interpretation of these results in terms of the effects of SARS-CoV-2 on the placenta and the pathophysiology of maternal-fetal infection. Placentas from pregnant women with COVID-19 and uninfected neonates show significant variability in the spectrum of pathology findings. In contrast, placentas from infected maternal-neonatal dyads are characterized by the finding of mononuclear cell inflammation of the intervillous space, termed chronic histiocytic intervillositis, together with syncytiotrophoblast necrosis. These placentas show prominent positivity of syncytiotrophoblast by SARS-CoV-2, fulfilling the published criteria for transplacental viral transmission as confirmed in fetal cells through identification of viral antigens by immunohistochemistry or viral nucleic acid using RNA in situ hybridization. The co-occurrence of chronic histiocytic intervillositis and trophoblast necrosis appears to be a risk factor for placental infection with SARS-CoV-2 as well as for maternal-fetal viral transmission, and suggests a potential mechanism by which the coronavirus can breach the maternal-fetal interface.

中文翻译:

有和没有胎儿和新生儿感染的COVID-19胎盘病理:滋养细胞坏死和慢性组织细胞间质炎是SARS-CoV-2经胎盘传播的危险因素

很大程度上未知的是,2019年冠状病毒疾病检测呈阳性的新生儿(COVID-19)感染的机制。已怀疑病原体SARS-CoV-2从母亲传播至婴儿,但难以确认。本交流根据婴儿的感染状况总结了COVID-19孕妇的病理发现范围,并就SARS-CoV-2对胎盘的作用和母体的病理生理学解释了这些结果的潜在解释。 -胎儿感染。患有COVID-19的孕妇胎盘和未感染的新生儿的胎盘在病理发现范围内显示出显着的变异性。相反,来自感染的母体-新生儿双胞胎的胎盘的特征是发现间质间隙的单核细胞发炎,称为慢性组织细胞间质炎,以及合体滋养层坏死。这些胎盘显示出SARS-CoV-2对合体滋养层细胞的突出阳性,符合通过胎盘细胞通过免疫组织化学或病毒核酸使用RNA原位杂交鉴定病毒抗原所证实的胎盘病毒传播标准。慢性组织细胞间质炎和滋养细胞坏死的并存似乎是SARS-CoV-2胎盘感染以及母婴病毒传播的危险因素,并暗示了冠状病毒可以破坏母源性病毒的潜在机制。胎儿界面。称为慢性组织细胞间质炎,以及合体滋养细胞坏死。这些胎盘表现出SARS-CoV-2的合体滋养层细胞突出的阳性,符合通过胎盘细胞通过免疫组织化学或病毒核酸使用RNA原位杂交鉴定病毒抗原所证实的胎盘病毒传播标准。慢性组织细胞间质炎和滋养细胞坏死的并存似乎是SARS-CoV-2胎盘感染以及母婴病毒传播的危险因素,并暗示了冠状病毒可以破坏母源性病毒的潜在机制。胎儿界面。称为慢性组织细胞间质炎,以及合体滋养细胞坏死。这些胎盘显示出SARS-CoV-2对合体滋养层细胞的突出阳性,符合通过胎盘细胞通过免疫组织化学或病毒核酸使用RNA原位杂交鉴定病毒抗原所证实的胎盘病毒传播标准。慢性组织细胞间质炎和滋养细胞坏死的并存似乎是SARS-CoV-2胎盘感染以及母婴病毒传播的危险因素,并暗示了冠状病毒可以破坏母源性病毒的潜在机制。胎儿界面。通过使用RNA原位杂交通过免疫组织化学或病毒核酸鉴定病毒抗原来满足胎儿细胞中证实的经胎盘病毒传播标准。慢性组织细胞间质炎和滋养细胞坏死的并存似乎是SARS-CoV-2胎盘感染以及母婴病毒传播的危险因素,并暗示了冠状病毒可以破坏母源性病毒的潜在机制。胎儿界面。通过使用RNA原位杂交通过免疫组织化学或病毒核酸鉴定病毒抗原来满足胎儿细胞中证实的经胎盘病毒传播标准。慢性组织细胞间质炎和滋养细胞坏死的并存似乎是SARS-CoV-2胎盘感染以及母婴病毒传播的危险因素,并暗示了冠状病毒可以破坏母源性病毒的潜在机制。胎儿界面。
更新日期:2020-11-15
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