Receptors in host pathogen interactions between human cytomegalovirus and the placenta during congenital infection

Abstract

Cellular receptors in human cytomegalovirus (HCMV) mother to child transmission play an important role in congenital infection. Placental trophoblast cells are a significant cell type in placental development, placental functional processes, and in HCMV transmission. Different cells within the placental floating and chorionic villi present alternate receptors for HCMV cell entry. Syncytiotrophoblasts present neonatal Fc receptors that bind and transport circulating maternal immunoglobulin G across the placental interface which can also be bound to HCMV virions, facilitating viral entry into the placenta and foetal circulation. Cytotrophoblast express HCMV receptors including integrin-α1β1, integrin-αVβ3, epidermal growth factor receptor and platelet-derived growth factor receptor alpha. The latter interacts with HCMV glycoprotein-H, glycoprotein-L and glycoprotein-O (gH/gL/gO) trimers (predominantly in placental fibroblasts) and the gH/gL/pUL128, UL130-UL131A pentameric complex in other placental cell types. The pentameric complex allows viral tropism of placental trophoblasts, endothelial cells, epithelial cells, leukocytes and monocytes. This review outlines HCMV ligands and target receptor proteins in congenital HCMV infection.

Constitutive Signaling by the Human Cytomegalovirus G Protein Coupled Receptor Homologs US28 and UL33 Enables Trophoblast Migration In Vitro

“…Human cytomegalovirus (HCMV) is the leading viral cause of congenital infection, resulting in fetal and neonatal death and neurodevelopmental and sensorineural sequelae [26]. HCMV spreads systemically and placental infection is likely initiated via infected maternal blood myeloid cells [50]. Within the placenta, trophoblast invasion, migration and fusion are highly coordinated events that are regulated by macrophage interactions [51].…”

Melatonin Alleviates Oxidative Stress Induced by H2O2 in Porcine Trophectoderm Cells

“…During pregnancy, the placenta is susceptible to oxidative stress and has a reduced antioxidant capacity, which can pose a potential problem for late animal reproduction and affect maternal homeostasis and fetal growth and development [ 3 , 4 , 5 ]. PTr2 cells are a significant cell type of the placenta, and they represent one of the earliest events of spectral differentiation in mammalian embryos [ 6 , 7 , 8 ]. Placental oxidative stress is involved in pregnancy complications, and previous studies have shown that oxidative stress of PTr2 cells can lead to pathological conditions of pregnancy (early pregnancy loss and impaired placentation) [ 9 , 10 ].…”