title: Cutting Edge: Fetal/Placental Type I IFN Can Affect Maternal Survival and Fetal Viral Load during Viral Infection.
abstract: Pregnant women have greater mortality and complications associated with viral infections compared with the general population, but the reason for the increased susceptibility is not well defined. Placenta type I IFN is an important immune modulator and protects the pregnancy. We hypothesized that loss of placental IFN affects the regulation of the maternal immune system, resulting in the differential response to infections observed in pregnancy. Pregnant mice lacking the IFN-α/β receptor (IFNAR) became viremic and had higher mortality compared with nonpregnant animals. Notably, an embryo with functional IFN signaling alone was sufficient to rescue the pregnant IFNAR-/-dam from virus-associated demise. Placental IFN was also an important regulator of viral replication in placental tissue and significantly affected viral transmission to the fetus. These findings highlight the role of fetal/placental IFN in the modulation of viral infection in the mother and fetus.
authors.affiliation: Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT 06520.|Department of Obstetrics, Gynecology, and Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, MI 49503.
authors.forename: Karen
authors.initials: K
authors.lastname: Racicot
authors.affiliation: Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT 06520.
authors.forename: Paulomi
authors.initials: P
authors.lastname: Aldo
authors.affiliation: Department of Pediatrics, Yale School of Medicine, New Haven, CT 06520.
authors.forename: Ayman
authors.identifier: 0000-0001-6118-6951
authors.initials: A
authors.lastname: El-Guindy
authors.affiliation: Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT 06520.|Department of Obstetrics and Gynecology, Institute of Women's Life Medical Science, Yonsei University College of Medicine, Seoul 120-749, Korea; and.
authors.forename: Ja-Young
authors.identifier: 0000-0003-3009-6325
authors.initials: JY
authors.lastname: Kwon
authors.affiliation: Perinatology Research Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Detroit, MI 48201.
authors.forename: Roberto
authors.identifier: 0000-0002-4448-5121
authors.initials: R
authors.lastname: Romero
authors.affiliation: Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT 06520; gil.mor@yale.edu.
authors.forename: Gil
authors.identifier: 0000-0002-5499-3912
authors.initials: G
authors.lastname: Mor
mesh_terms: D000818:Animals; D005260:Female; D005333:Fetus / Q000276:immunology*; D005838:Genotype; D006566:Herpesviridae Infections / Q000276:immunology*; D007370:Interferon Type I / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010920:Placenta / Q000276:immunology*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology*; D018144:Rhadinovirus / Q000276:immunology; D014412:Tumor Virus Infections / Q000276:immunology; D019562:Viral Load
chemical_list: D007370:Interferon Type I