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Coronavirus disease 2019 and the placenta: A literature review.
Placenta. 2022 08; 126:209-223.P

Abstract

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has been implicated in the clinical pathology of multiple organs and organ systems. Due to the novelty of the disease, there is a need to review emerging literature to understand the profile of SARS-CoV-2 in the placenta. This review sought to evaluate the literature on the mediators, mechanism of entry, pathogenesis, detection, and pathology of SARS-CoV-2 in the placenta. Systematic literature searches found 96 eligible studies. Our review revealed that SARS-CoV-2 canonical mediators, angiotensin-converting enzyme-2 (ACE2), and transmembrane serine protease-2 (TMPRSS2) are variably expressed in various placenta compartments, including the villous cytotrophoblasts, syncytiotrophoblasts (STBs), and extravillous trophoblasts (EVTs) throughout pregnancy. Placental SARS-CoV-2 and coronavirus-associated receptors and factors (SCARFs), including basigin (BSG/CD147), dipeptidyl peptidase-4 (DPP4/CD26), cathepsin B/L (CTL B/L), furin, interferon-induced transmembrane protein (IFITM1-3), and lymphocyte antigen 6E (LY6E) may increase or reduce the permissiveness of the placenta to SARS-CoV-2. EVTs express genes that code for proteins that may drive viral pathogenesis in the placenta. Viral RNA, proteins, and particles were detected primarily in the STBs by in situ hybridization, immunohistochemistry, electron microscopy, and polymerase chain reaction. Placental pathology in SARS-CoV-2-infected placentas included maternal and fetal vascular malperfusion and a generally nonspecific inflammatory-immune response. The localization of SARS-CoV-2 receptors, proteases, and genes involved in coding proteins that drive viral pathogenesis in the placenta predisposes the placenta to SARS-CoV-2 infection variably in all pregnancy trimesters, with antecedent placental pathology. There is a need for further studies to explicate the mechanism of entry and pathogenesis of SARS-CoV-2 in the placenta.

Authors+Show Affiliations

Basic Clinical and Translational (BCT) Research Laboratory, University of Nairobi, Nairobi, Kenya. Electronic address: gesakarema@gmx.com.Basic Clinical and Translational (BCT) Research Laboratory, University of Nairobi, Nairobi, Kenya; Department of Human Anatomy, University of Nairobi, Nairobi, Kenya; Department of Obstetrics and Gynecology, University of Nairobi, Nairobi, Kenya. Electronic address: obimbomad@gmail.com.Basic Clinical and Translational (BCT) Research Laboratory, University of Nairobi, Nairobi, Kenya; Department of Obstetrics and Gynecology, Kenyatta University, Nairobi, Kenya. Electronic address: Wanyoro.Anthony@ku.ac.ke.

Pub Type(s)

Journal Article
Review
Systematic Review

Language

eng

PubMed ID

35872511

Citation

Gesaka, Samwel R., et al. "Coronavirus Disease 2019 and the Placenta: a Literature Review." Placenta, vol. 126, 2022, pp. 209-223.
Gesaka SR, Obimbo MM, Wanyoro A. Coronavirus disease 2019 and the placenta: A literature review. Placenta. 2022;126:209-223.
Gesaka, S. R., Obimbo, M. M., & Wanyoro, A. (2022). Coronavirus disease 2019 and the placenta: A literature review. Placenta, 126, 209-223. https://doi.org/10.1016/j.placenta.2022.07.007
Gesaka SR, Obimbo MM, Wanyoro A. Coronavirus Disease 2019 and the Placenta: a Literature Review. Placenta. 2022;126:209-223. PubMed PMID: 35872511.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Coronavirus disease 2019 and the placenta: A literature review. AU - Gesaka,Samwel R, AU - Obimbo,Moses M, AU - Wanyoro,Anthony, Y1 - 2022/07/19/ PY - 2021/12/29/received PY - 2022/07/13/accepted PY - 2022/7/26/pubmed PY - 2022/8/17/medline PY - 2022/7/25/entrez KW - ACE2 KW - Placental infection KW - Placental pathology KW - SARS-CoV-2 KW - Single-cell analysis SP - 209 EP - 223 JF - Placenta JO - Placenta VL - 126 N2 - Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has been implicated in the clinical pathology of multiple organs and organ systems. Due to the novelty of the disease, there is a need to review emerging literature to understand the profile of SARS-CoV-2 in the placenta. This review sought to evaluate the literature on the mediators, mechanism of entry, pathogenesis, detection, and pathology of SARS-CoV-2 in the placenta. Systematic literature searches found 96 eligible studies. Our review revealed that SARS-CoV-2 canonical mediators, angiotensin-converting enzyme-2 (ACE2), and transmembrane serine protease-2 (TMPRSS2) are variably expressed in various placenta compartments, including the villous cytotrophoblasts, syncytiotrophoblasts (STBs), and extravillous trophoblasts (EVTs) throughout pregnancy. Placental SARS-CoV-2 and coronavirus-associated receptors and factors (SCARFs), including basigin (BSG/CD147), dipeptidyl peptidase-4 (DPP4/CD26), cathepsin B/L (CTL B/L), furin, interferon-induced transmembrane protein (IFITM1-3), and lymphocyte antigen 6E (LY6E) may increase or reduce the permissiveness of the placenta to SARS-CoV-2. EVTs express genes that code for proteins that may drive viral pathogenesis in the placenta. Viral RNA, proteins, and particles were detected primarily in the STBs by in situ hybridization, immunohistochemistry, electron microscopy, and polymerase chain reaction. Placental pathology in SARS-CoV-2-infected placentas included maternal and fetal vascular malperfusion and a generally nonspecific inflammatory-immune response. The localization of SARS-CoV-2 receptors, proteases, and genes involved in coding proteins that drive viral pathogenesis in the placenta predisposes the placenta to SARS-CoV-2 infection variably in all pregnancy trimesters, with antecedent placental pathology. There is a need for further studies to explicate the mechanism of entry and pathogenesis of SARS-CoV-2 in the placenta. SN - 1532-3102 UR - https://www.unboundmedicine.com/medline/citation/35872511/Coronavirus_disease_2019_and_the_placenta:_A_literature_review_ DB - PRIME DP - Unbound Medicine ER -