Objective
Infection of pregnant women during previous coronavirus mediated pandemics such as Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS), were associated with high rates of fetal and maternal demise. However, the characteristics of COVID-19 in pregnant and non-pregnant women are very similar and while severe COVID-19 in pregnancy brings increased risk of preterm birth and intensive care admission 1 most pregnant women, be they symptomatic or asymptomatic for SARS-CoV-2 infection, do not experience severe complications in pregnancy 2. Similarly, cases of SARS-CoV-2 vertical transmission are rare and there is low risk of serious disease for the neonate 3. Understanding the mechanisms of resilience against severe COVID-19 in pregnant women and the newborn are critical to ensure ongoing vigilance in care and to provide insight into disease pathogenesis and therapeutic opportunities.
Angiotensin-converting enzyme 2 (ACE2), CD26, CD147 and neuropilin-1 (NRP-1) are some of the key molecules identified as contributing to the entry of coronaviruses such as SARS-CoV-2 into human cells4. There is immense interest in these and viral entry facilitating proteases such as transmembrane serine protease-2 (TMPRSS2) as therapeutic targets for limiting infection. Soluble forms of viral entry receptors have been postulated to act as viral traps for SARS-CoV-2 by preventing interaction of the virus with membrane-bound forms 5. We predict that elevation of these at the maternal-fetal interface contributes to the lack of vertical transmission and limits severity of disease from SARS-CoV-2 infection in the fetus and neonate.
Hypothesis : Soluble (s) ACE2, sCD26, sCD147 and sNRP-1 are elevated at the maternal-fetal interface.