Abstract
BackgroundPregnant 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.MethodsWe 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.FindingsTMPRSS2 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.InterpretationThis 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 abstractThis 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.
Highlights
The COVID-19 pandemic has brought about unprecedented research efforts in attempts to prevent and treat infection across all ages
This analysis indicated that while other tissues, notably kidney and lung, showed expression of ACE2, the lack of co-expression with TMPRSS2 suggests these tissues are unlikely to be susceptible to SARS-CoV-2 infection during gestation
Coexpression of ACE2 and TMPRSS2 in the intestine increased during gestation in an exponential manner across the first and second trimester timepoints studied (10 to 18 PCW)
Summary
The COVID-19 pandemic has brought about unprecedented research efforts in attempts to prevent and treat infection across all ages. Recent data suggest that the fetus may have some susceptibility to SARS-CoV-2 infection[3,4,5], alongside a plausible increased risk of preterm birth. These observed risks appear to relate to the severity of maternal infection, and documented placental pathology has been reported to correlate with severe maternal symptoms[6,7]. We validated our findings by exploring gene expression levels of ACE2 and TMPRSS2 via quantitative PCR analysis of the fetal tissues that could be exposed to virus in utero and examined expression at protein level using multicolour immunohistochemistry. The data were validated at both gene and protein level by performing RT-qPCR and two-colour immunohistochemistry on a library of second-trimester human fetal tissues
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