Authors: Ouyang, Yingshi; Bagalkot, Tarique; Fitzgerald, Wendy; Sadovsky, Elena; Chu, Tianjiao; Martínez-Marchal, Ana; Brieño-Enríquez, Miguel; Su, Emily J.; Margolis, Leonid; Sorkin, Alexander; Sadovsky, Yoel
Online: https://journals.asm.org/doi/abs/10.1128/mSphere.00250-21
Issue: mSphere. 2021 Apr 14;6(2):e00250-21.
Abstract
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has had a massive impact on human lives worldwide. While the airborne SARS-CoV-2 primarily affects the lungs, viremia is not uncommon. As placental trophoblasts are directly bathed in maternal blood, they are vulnerable to SARS-CoV-2. Intriguingly, the human fetus is largely spared from SARS-CoV-2 infection. We tested whether the human placenta expresses the main SARS-CoV-2 entry factors angiotensin-converting enzyme 2 (ACE2), transmembrane protease serine 2 (TMPRSS2), and furin and showed that ACE2 and TMPRSS2 are expressed in the trophoblast rather than in other placental villous cells. While furin is expressed in the main placental villous cell types, we surveyed, trophoblasts exhibit the highest expression. In line with the expression of these entry factors, we demonstrated that a SARS-CoV-2 pseudovirus could enter primary human trophoblasts. Mechanisms underlying placental defense against SARS-CoV-2 infection likely involve postentry processing, which may be germane for mitigating interventions against SARS-CoV-2.
