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  • nrc
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  • Research Engineer
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  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
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Published in Science (New York, N.Y.) - 12 Jul 2019

Buchrieser J, Degrelle SA, Couderc T, Nevers Q, Disson O, Manet C, Donahue DA, Porrot F, Hillion KH, Perthame E, Arroyo MV, Souquere S, Ruigrok K, Dupressoir A, Heidmann T, Montagutelli X, Fournier T, Lecuit M, Schwartz O,

Link to Pubmed [PMID] – 31296770

Link to DOI – 10.1126/science.aaw7733

Science 2019 Jul; 365(6449): 176-180

Elevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes. Using cultures of human trophoblasts or mouse cells, we show that IFN-induced transmembrane proteins (IFITMs), a family of restriction factors blocking the entry step of many viruses, impair ST formation and inhibit syncytin-mediated fusion. Moreover, the IFN inducer polyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but not in Ifitm-deleted mice. Thus, excessive levels of IFITMs may mediate the pregnancy complications observed during congenital infections and other IFN-induced pathologies.