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Published on: January 9, 2019
Term Human Placental Trophoblasts Express SARS-CoV-2 Entry Factors ACE2, TMPRSS2, and Furin
Yingshi Ouyang1, Tarique Bagalkot2, Wendy Fitzgerald3
1Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA ouyangy@mwri.magee.edu sorkin@pitt.edu ysadovsky@mwri.magee.edu.
The human placenta expresses key SARS-CoV-2 entry factors, ACE2 and TMPRSS2, in trophoblasts, allowing viral entry. However, the fetus is largely protected, suggesting placental defense mechanisms against COVID-19 infection.
Area of Science:
- Virology
- Immunology
- Reproductive Biology
Background:
- The COVID-19 pandemic, caused by SARS-CoV-2, poses risks to pregnant women.
- While SARS-CoV-2 primarily affects the lungs, viremia can occur, potentially exposing the placenta.
- The human fetus appears largely protected from SARS-CoV-2 infection despite potential placental exposure.
Purpose of the Study:
- To investigate the expression of SARS-CoV-2 entry factors (ACE2, TMPRSS2, furin) in the human placenta.
- To determine if primary human trophoblasts are susceptible to SARS-CoV-2 entry.
Main Methods:
- Transcriptome sequencing (RNA-seq)
- Real-time quantitative PCR (RT-qPCR)
- In situ hybridization
- Immunofluorescence
- SARS-CoV-2 pseudovirus entry assay
Main Results:
- ACE2 and TMPRSS2 are expressed in placental trophoblasts, not other villous cells.
- Furin is broadly expressed across placental villous cell types, with highest expression in trophoblasts.
- Primary human trophoblasts are permissive to SARS-CoV-2 pseudovirus entry.
Conclusions:
- The human placenta expresses key SARS-CoV-2 entry factors in trophoblasts.
- Trophoblasts are susceptible to SARS-CoV-2 entry, supporting potential feto-placental infection.
- Mechanisms of placental defense against SARS-CoV-2 likely involve post-entry processes.
