Abstract：
SARS-CoV-2 infection during pregnancy may cause viral inflammation of the placenta, resulting in fetal demise even without fetal or newborn infection. The impact of timing of the infection and the mechanisms that cause fetal morbidity and mortality are not well understood.
To describe placental pathology from women with confirmed SARS-CoV-2 infection during pregnancy, a SARS-CoV-2 immunohistochemistry-positive placenta and late miscarriage, stillbirth, neonatal death, or medically indicated birth due to fetal distress.
The triad of trophoblastic necrosis, inflammatory intervillous infiltrates, and increased perivillous fibrinoid deposition was present in all 17 placentas; the pregnancies resulted in eight stillbirths, two late miscarriages (19 and 21 weeks\' gestation), and seven liveborn children, two of which died shortly after delivery. The severity of maternal COVID-19 was not reflected by the extent of the placental lesions. In only one case, SARS-CoV-2 was detected in lung tissue samples from the fetus. The majority events (miscarriage, stillbirth, fetal distress resulting in indicated birth, or livebirth, but neonatal death) happened shortly after maternal SARS-CoV-2 infection was diagnosed. Seven of eight sequenced cases were infected with the Delta (B.1.617.2) virus strain.
We consolidate findings from previous case series describing extensive SARS-CoV-2 placentitis and placental insufficiency leading to fetal hypoxia. We found sparse evidence to support the notion that SARS-CoV-2 virus had infected the fetus or newborn.
To describe placental pathology from women with confirmed SARS-CoV-2 infection during pregnancy, a SARS-CoV-2 immunohistochemistry-positive placenta and late miscarriage, stillbirth, neonatal death, or medically indicated birth due to fetal distress.
The triad of trophoblastic necrosis, inflammatory intervillous infiltrates, and increased perivillous fibrinoid deposition was present in all 17 placentas; the pregnancies resulted in eight stillbirths, two late miscarriages (19 and 21 weeks\' gestation), and seven liveborn children, two of which died shortly after delivery. The severity of maternal COVID-19 was not reflected by the extent of the placental lesions. In only one case, SARS-CoV-2 was detected in lung tissue samples from the fetus. The majority events (miscarriage, stillbirth, fetal distress resulting in indicated birth, or livebirth, but neonatal death) happened shortly after maternal SARS-CoV-2 infection was diagnosed. Seven of eight sequenced cases were infected with the Delta (B.1.617.2) virus strain.
We consolidate findings from previous case series describing extensive SARS-CoV-2 placentitis and placental insufficiency leading to fetal hypoxia. We found sparse evidence to support the notion that SARS-CoV-2 virus had infected the fetus or newborn.
摘要：
背景：妊娠期SARS-CoV-2感染可能引起胎盘病毒性炎症，即使没有胎儿或新生儿感染，也会导致胎儿死亡。感染时机的影响以及导致胎儿发病和死亡的机制尚不清楚。
方法：描述妊娠期间确诊SARS-CoV-2感染妇女的胎盘病理，SARS-CoV-2免疫组织化学阳性胎盘和晚期流产，死产,新生儿死亡,或医学上表明由于胎儿窘迫而出生。
结果：滋养细胞坏死三联征，炎性绒毛间浸润，在所有17个胎盘中都存在增加的绒毛周围纤维蛋白样沉积；怀孕导致8例死产，两次晚期流产（妊娠19周和21周），和七个活着出生的孩子，其中两人在分娩后不久死亡。母体COVID-19的严重程度没有反映在胎盘病变的程度上。只有一种情况,在胎儿的肺组织样本中检测到SARS-CoV-2。大多数事件(流产，死产,胎儿窘迫导致指示出生，或者活产，但是新生儿死亡）在诊断出孕产妇SARS-CoV-2感染后不久发生。8例测序病例中有7例感染了Delta（B.1.617.2）病毒株。
结论：我们巩固了先前病例系列的发现，描述了广泛的SARS-CoV-2胎盘炎和胎盘功能不全导致胎儿缺氧。我们发现很少的证据支持SARS-CoV-2病毒感染胎儿或新生儿的观点。
方法：描述妊娠期间确诊SARS-CoV-2感染妇女的胎盘病理，SARS-CoV-2免疫组织化学阳性胎盘和晚期流产，死产,新生儿死亡,或医学上表明由于胎儿窘迫而出生。
结果：滋养细胞坏死三联征，炎性绒毛间浸润，在所有17个胎盘中都存在增加的绒毛周围纤维蛋白样沉积；怀孕导致8例死产，两次晚期流产（妊娠19周和21周），和七个活着出生的孩子，其中两人在分娩后不久死亡。母体COVID-19的严重程度没有反映在胎盘病变的程度上。只有一种情况,在胎儿的肺组织样本中检测到SARS-CoV-2。大多数事件(流产，死产,胎儿窘迫导致指示出生，或者活产，但是新生儿死亡）在诊断出孕产妇SARS-CoV-2感染后不久发生。8例测序病例中有7例感染了Delta（B.1.617.2）病毒株。
结论：我们巩固了先前病例系列的发现，描述了广泛的SARS-CoV-2胎盘炎和胎盘功能不全导致胎儿缺氧。我们发现很少的证据支持SARS-CoV-2病毒感染胎儿或新生儿的观点。
