Debelenko Larisa
Department of Pathology and Cell Biology, Columbia University-Irving Medical Center, New York, NY 10032, USA.
J Dev Biol. 2023 Nov 16;11(4):42. doi: 10.3390/jdb11040042.
This review focuses on SARS-CoV-2 infection in placental and fetal tissues. Viremia is rare in infected pregnant women, and the virus is seldom amplified from placental tissues. Definite and probable placental infection requires the demonstration of viral RNA or proteins using in situ hybridization (ISH) and immunohistochemistry (IHC). Small subsets (1.0-7.9%, median 2.8%) of placentas of SARS-CoV-2-positive women showed definite infection accompanied by a characteristic histopathology named SARS-CoV-2 placentitis (SP). The conventionally accepted histopathological criteria for SP include the triad of intervillositis, perivillous fibrin deposition, and trophoblast necrosis. SP was shown to be independent of the clinical severity of the infection, but associated with stillbirth in cases where destructive lesions affecting more than 75% of the placental tissue resulted in placental insufficiency and severe fetal hypoxic-ischemic injury. An association between maternal thrombophilia and SP was shown in a subset of cases, suggesting a synergy of the infection and deficient coagulation cascade as one of the mechanisms of the pathologic accumulation of fibrin in affected placentas. The virus was amplified from fetal tissues in approximately 40% of SP cases, but definite fetal involvement demonstrated using ISH or IHC is exceptionally rare. The placental pathology in SARS-CoV-2-positive women also includes chronic lesions associated with placental malperfusion in the absence of definite or probable placental infection. The direct viral causation of the vascular malperfusion of the placenta in COVID-19 is debatable, and common predispositions (hypertension, diabetes, and obesity) may play a role.
本综述聚焦于严重急性呼吸综合征冠状病毒2（SARS-CoV-2）在胎盘和胎儿组织中的感染情况。病毒血症在感染的孕妇中较为罕见，且病毒很少能从胎盘组织中扩增出来。明确和可能的胎盘感染需要通过原位杂交（ISH）和免疫组织化学（IHC）来证明病毒RNA或蛋白质的存在。SARS-CoV-2阳性女性的小部分胎盘（1.0 - 7.9%，中位数为2.8%）显示出明确感染，并伴有一种名为SARS-CoV-2胎盘炎（SP）的特征性组织病理学表现。SP传统上公认的组织病理学标准包括绒毛间炎、绒毛周围纤维蛋白沉积和滋养层坏死三联征。SP被证明与感染的临床严重程度无关，但在破坏性病变影响超过75%的胎盘组织导致胎盘功能不全和严重胎儿缺氧缺血性损伤的情况下，与死产有关。在一部分病例中显示母体血栓形成倾向与SP有关，提示感染与凝血级联缺陷的协同作用是受影响胎盘中纤维蛋白病理积聚的机制之一。在大约40%的SP病例中，病毒能从胎儿组织中扩增出来，但使用ISH或IHC证明胎儿明确受累的情况极为罕见。SARS-CoV-2阳性女性的胎盘病理学还包括在没有明确或可能的胎盘感染时与胎盘灌注不良相关的慢性病变。COVID-19中胎盘血管灌注不良的直接病毒病因存在争议，常见的易患因素（高血压、糖尿病和肥胖）可能起作用。
