Cellular and molecular mechanisms of viral infection in the human placenta

Abstract

The placenta is a highly specialized organ that is formed during human gestation for conferring protection and generating an optimal microenvironment to maintain the equilibrium between immunological and biochemical factors for fetal development. Diverse pathogens, including viruses, can infect several cellular components of the placenta, such as trophoblasts, syncytiotrophoblasts and other hematopoietic cells. Viral infections during pregnancy have been associated with fetal malformation and pregnancy complications such as preterm labor. In this minireview, we describe the most recent findings regarding virus-host interactions at the placental interface and investigate the mechanisms through which viruses may access trophoblasts and the pathogenic processes involved in viral dissemination at the maternal-fetal interface.

Placental Cytopathic Damage Factor Due to Parvovirus B19 – As a Hallmark of Intrauterine Symptomathy of Infected Fetus

“…19-infected erythroblast cells with intranuclear inclusions have been observed in placenta and fetal tissue by many authors with histology and electron microscopy methods [1,3,5]. In our research the histopathological assessment of placenta in case of parvovirus infection is characterized by pronounced placentitis with edema due to the cytolytic action of viruses in the core of endothelial cells of the blood capillaries, as well as in the cytoplasm, myelin-like structures, which contributes to the enhancement of lipid peroxide oxidation.…”

“…Transmission of virus may occur not only through damage in the protective placental barrier, but also through endocytosis or receptor-mediated transfer. The mechanism by which the virus can be transmitted from the infected mother to the fetus was studied using experimental models which found that immunoreactivity for B19 infection was most pronounced in the sponged trophoblastic placental cells in the first trimester; reduction in reactivity was observed in the placenta cells in the second trimester, but almost no coloration of the antigen was noted in the third trimester [5]. The reason for this difference for fetal effects is not only the presence of a greater number of target cells during the first and second trimester, but also a greater number of viral receptors on the spider trophoblast layer of the placenta.…”

Recent Updates on Research Models and Tools to Study Virus–Host Interactions at the Placenta

“…The placenta is assembled by the chorionic villi, which comprise floating villi and anchoring villi. The floating villi are mainly responsible for transporting waste, nutrients, and gases between the mother and the fetus, while the anchoring villi support the decidua [9]. Various subsets of maternal immune cells constitute the decidual immune system, such as macrophages, dendritic cells, natural killer cells, and T cells [10].…”

“…While CTBs form the anchoring villi, STBs form the floating villi and are responsible for the exchange that occurs at the villus surface between maternal blood and fetus [13]. Aggregates of CTBs also organize into extravillous cytotrophoblasts (EVTs), which are placental trophoblasts that invade the maternal decidua, anchor the placenta, and subsequently lead to the transfer of nutrients to the fetus [9,14]. In addition to separating the fetus from maternal tissues, the layer composed of STBs and CTBs is particularly important in terms of protecting the semi-allogenic fetus against maternal immune attacks [15].…”

Cytoplasmic m1A reader YTHDF3 inhibits trophoblast invasion by downregulation of m1A-methylated IGF1R

“…Recent transcriptome-wide mapping also revealed that m 1 A modification is also present in human messenger RNAs (mRNAs) and suggested the potential roles of m 1 A in modulating mRNA splicing and translation; meanwhile, m 1 A modification is dynamically changed upon external heat or starve stimulation [8][9][10] . Maternal-fetal interface cells would suffer many external stimuli (hypoxia, lipopolysaccharide (LPS), and hormone), which dynamically changed during the pregnancy, especially the hypoxia environment could affect trophoblast activity [11][12][13] . However, whether the trophoblast has dynamic m 1 A modification upon hypoxia remains unclear.…”