Vertical transmission of SARS‐CoV2 during pregnancy: A high‐risk cohort

Maeda, Mariane de Fátima Yukie; Brizot, Maria de Lourdes; Gibelli, Maria Augusta Bento Cicaroni; Ibidi, Silvia Maria; Carvalho, Werther Brunow de; Hoshida, Mara Sandra; Machado, Clarisse Martins; Sabino, Éster Cerdeira; Silva, Lea Campos de Oliveira da; Jaenisch, Thomas; Mendes-Corrêa, Maria Cássia; Mayaud, Philippe; Francisco, Rossana Pulcinelli Vieira

doi:10.1002/pd.5980

Cited by 32 publications

(38 citation statements)

References 30 publications

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“… 42 , 43 However, given the immunological changes occurring around the time of labour, 44 we would suggest that there is currently inadequate evidence to rule this out as the potential route for infection of neonates who are known to have been infected. 3 , 4 , 5 In conclusion, we would propose that maternal viraemia‐associated presence of virus within the amniotic fluid and birth canal, as reported, 28 , 33 may produce an environment where the fetus is susceptible to infection through the gastrointestinal tract, and that this susceptibility may be present from the late second trimester.…”

Section: Discussionmentioning

confidence: 79%

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COVID‐19 and vertical transmission: assessing the expression of ACE2/TMPRSS2 in the human fetus and placenta to assess the risk of SARS‐CoV‐2 infection

Beesley

Davidson

Panariello

et al. 2021

BJOG

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Background Pregnant women have been identified as a potentially at‐risk group concerning COVID‐19 infection, but little is known regarding the susceptibility of the fetus to infection. Co‐expression of ACE2 and TMPRSS2 has been identified as a prerequisite for infection, and expression across different tissues is known to vary between children and adults. However, the expression of these proteins in the fetus is unknown. Methods We performed a retrospective analysis of a single cell data repository. The data were then validated at both gene and protein level by performing RT‐qPCR and two‐colour immunohistochemistry on a library of second‐trimester human fetal tissues. Findings TMPRSS2 is present at both gene and protein level in the predominantly epithelial fetal tissues analysed. ACE2 is present at significant levels only in the fetal intestine and kidney, and is not expressed in the fetal lung. The placenta also does not co‐express the two proteins across the second trimester or at term. Interpretation This dataset indicates that the lungs are unlikely to be a viable route of SARS‐CoV2 fetal infection. The fetal kidney, despite presenting both the proteins required for the infection, is anatomically protected from the exposure to the virus. However, the gastrointestinal tract is likely to be susceptible to infection due to its high co‐expression of both proteins, as well as its exposure to potentially infected amniotic fluid. Tweetable abstract This work provides detailed mechanistic insight into the relative protection & vulnerabilities of the fetus & placenta to SARS‐CoV‐2 infection by scRNAseq & protein expression analysis for ACE2 & TMPRSS2. The findings help to explain the low rate of vertical transmission.

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Section: Discussionmentioning

confidence: 79%

“…There have been speculative data published suggesting that women may be at risk of severe SARS‐CoV2‐related illness in the peripartum period, which has led to regional policy that the non‐compromised fetus should remain undelivered if possible. 32 , 33 …”

Section: Discussionmentioning

confidence: 99%

COVID‐19 and vertical transmission: assessing the expression of ACE2/TMPRSS2 in the human fetus and placenta to assess the risk of SARS‐CoV‐2 infection

Beesley

Davidson

Panariello

et al. 2021

BJOG

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“…However, despite a lack of maternal severe disease, 50% ( n = 2) of the women showed signs of systemic SARS-CoV-2 presence based on maternal viremia and vaginal fornix SARS-CoV-2 positivity ( Table 4 ). All cases hospitalized for severe disease and an associated increased risk for maternal viremia [ 19 , 21 ], had negative SARS-CoV-2 PCRs in maternal blood or fornix posterior, showed negative immunohistochemical staining for SARS-CoV-2 of the placenta and did not have severe inflammatory abnormalities in the placenta.…”

Section: Resultsmentioning

confidence: 99%

“…Still, despite this finding maternal viremia or placental infection was initially thought not to be a major issue as published in a prospective cohort study in 2020 [ 20 ]. However, a recent study in symptomatic pregnant women admitted at the hospital for COVID-19 related symptoms, showed that maternal viremia was associated with SARS-CoV-2 presence in the foetal compartment [ 21 ], hence indicative of transplacental transmission of SARS-CoV-2. Maternal viremia seems imperative to allow placental infection by SARS-CoV-2.…”

Section: Introductionmentioning

confidence: 99%

Unique Severe COVID-19 Placental Signature Independent of Severity of Clinical Maternal Symptoms

Husen

Meeren

Verdijk

et al. 2021

Viruses

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Background: Although the risk for transplacental transmission of SARS-CoV-2 is rare, placental infections with adverse functional consequences have been reported. This study aims to analyse histological placental findings in pregnancies complicated by SARS-CoV-2 infection and investigate its correlation with clinical symptoms and perinatal outcomes. We want to determine which pregnancies are at-risk to prevent adverse pregnancy outcomes related to COVID-19 in the future. Methods: A prospective, longitudinal, multicentre, cohort study. All pregnant women presenting between April 2020 and March 2021 with a nasopharyngeal RT-PCR-confirmed SARS-CoV-2 infection were included. Around delivery, maternal, foetal and placental PCR samples were collected. Placental pathology was correlated with clinical maternal characteristics of COVID-19. Results: Thirty-six patients were included, 33 singleton pregnancies (n = 33, 92%) and three twin pregnancies (n = 3, 8%). Twenty-four (62%) placentas showed at least one abnormality. Four placentas (4/39, 10%) showed placental staining positive for the presence of SARS-CoV-2 accompanied by a unique combination of diffuse, severe inflammatory placental changes with massive perivillous fibrin depositions, necrosis of syncytiotrophoblast, diffuse chronic intervillositis, and a specific, unprecedented CD20+ B-cell infiltration. This SARS-CoV-2 placental signature seems to correlate with foetal distress (75% vs. 15.6%, p = 0·007) but not with the severity of maternal COVID-19 disease. Conclusion: We describe a unique placental signature in pregnant patients with COVID-19, which has not been reported in a historical cohort. We show that the foetal environment can be seriously compromised by disruption of placental function due to local, devastating SARS-CoV-2 infection. Maternal clinical symptoms did not predict the severity of the SARS-CoV-2-related placental signature, resulting in a lack of adequate identification of maternal criteria for pregnancies at risk. Close foetal monitoring and pregnancy termination in case of foetal distress can prevent adverse pregnancy outcomes due to COVID-19 related placental disease.

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“…This reduction was dependent on the timepoint of infection, indicating that the most significant results occurred in the third trimester, thereby overlapping with the saccular stage of lung development dedicated to the expansion of (future) air spaces. 5 Despite equivocal findings on placental transmission, 6 predominant viral transmission in the third trimester, 1 and the significant correlation between positive maternal PCR test and amniotic presence of SARS-CoV-2 near term 7 might enhance exposure of the developing lung parenchyma to the virus, facilitated through increased fetal breathing in the third trimester. Specifically, the high affinity of the virus to alveolar epithelial cells 3 could affect the so-called developmental sprint of these cells.…”

mentioning

confidence: 99%