학술논문
Chronic Histiocytic Intervillositis With Trophoblast Necrosis Is a Risk Factor Associated With Placental Infection From Coronavirus Disease 2019 (COVID-19) and Intrauterine Maternal-Fetal Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Transmission in Live-Born and Stillborn Infants.
Document Type
Article
Author
Schwartz, David A.; Baldewijns, Marcella; Benachi, Alexandra; Bugatti, Mattia; Collins, Rebecca R. J.; De Luca, Danièle; Facchetti, Fabio; Linn, Rebecca L.; Marcelis, Lukas; Morotti, Denise; Morotti, Raffaella; Parks, W. Tony; Patanè, Luisa; Prevot, Sophie; Pulinx, Bianca; Rajaram, Veena; Strybol, David; Thomas, Kristen; Vivanti, Alexandre J.
Source
Subject
*BLASTOCYST
*COMMUNICABLE diseases
*COVID-19
*IMMUNOHISTOCHEMISTRY
*RETROSPECTIVE studies
*RNA
*PREGNANCY complications
*CASE studies
*IN situ hybridization
*NECROSIS
*VERTICAL transmission (Communicable diseases)
*DISEASE risk factors
*PREGNANCY
*
*
*
*
*
*
*
*
*
*
*
*
Language
ISSN
0003-9985
Abstract
* Context.--The number of neonates with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is increasing, and in a few there are reports of intrauterine infection. Objective.--To characterize the placental pathology findings in a preselected cohort of neonates infected by transplacental transmission arising from maternal infection with SARS-CoV-2, and to identify pathology risk factors for placental and fetal infection. Design.--Case-based retrospective analysis by a multinational group of 19 perinatal specialists of the placental pathology findings from 2 cohorts of infants delivered to mothers testing positive for SARS-CoV-2: live-born neonates infected via transplacental transmission who tested positive for SARS-CoV-2 after delivery and had SARS-CoV-2 identified in cells of the placental fetal compartment by molecular pathology, and stillborn infants with syncytiotrophoblast positive for SARS-CoV-2. Results.--In placentas from all 6 live-born neonates acquiring SARS-CoV-2 via transplacental transmission, the syncytiotrophoblast was positive for coronavirus using immunohistochemistry, RNA in situ hybridization, or both. All 6 placentas had chronic histiocytic intervillositis and necrosis of the syncytiotrophoblast. The 5 stillborn/terminated infants had placental pathology findings that were similar, including SARS-CoV-2 infection of the syncytiotrophoblast, chronic histiocytic intervillositis, and syncytiotrophoblast necrosis. Conclusions.--Chronic histiocytic intervillositis together with syncytiotrophoblast necrosis accompanies SARS-CoV-2 infection of syncytiotrophoblast in live-born and stillborn infants. The coexistence of these 2 findings in all placentas from live-born infants acquiring their infection prior to delivery indicates that they constitute a pathology risk factor for transplacental fetal infection. Potential mechanisms of infection of the placenta and fetus with SARSCoV-2, and potential future studies, are discussed. [ABSTRACT FROM AUTHOR]