Buchrieser et al found that interferon, a molecule produced particularly in response to viral infection, may be responsible for abnormalities in placental development. Interferon-induced transmembrane proteins (IFITMs) were found to inhibit syncytin, restricting the fusion of trophoblast cells into a multi-nucleated syncytiotrophoblast layer (ST) and preventing the formation of the external layer of the placenta. This leads to poor placental development, triggering foetal demise. The study showed that excessive levels of IFITMs may mediate pregnancy complications observed during congenital infections and other IFN-induced pathologies. Using cultures of human trophoblasts or mouse cells, the researchers showed that IFN-induced transmembrane proteins (IFITMs), induced in presence of interferons, impaired ST formation and inhibit syncytin-mediated fusion. The results provide a molecular explanation for placental dysfunctions observed in interferon-mediated disorders, such as intrauterine growth retardation, TORCH (toxoplasmosis, other, rubella, cytomegalovirus, and herpes) infections, and some forms of preeclampsia.
Source: Science 12 Jul 2019: Vol. 365, Issue 6449, pp. 176-180 DOI: 10.1126/science.aaw7733 https://science.sciencemag.org/content/365/6449/176.editor-summary