Briah Barksdale
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Briah Barksdale has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
Alexandra H. Lopez
Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, USA
1 shared publication- Christopher A. Hunter
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania
1 shared publication Drake T. Philip
Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, USA
1 shared publication- Kellie Ann Jurado
Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, 19104, United States of America
1 shared publication - Madeline S. Merlino
Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, USA
1 shared publication Monica N. Mainigi
Department of Obstetrics and Gynecology, Hospital at the University of Pennsylvania, Philadelphia, USA
1 shared publication
Latest Publications
- Open Access
- 19 December 2025
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Interleukin-27 is antiviral against Zika virus at the maternal-fetal interface
Congenital viral infections can have severe consequences for pregnancy and fetal outcomes. Remarkably, the fetal-derived placenta serves as a robust barrier to infection through meticulous regulation by immune effectors and cytokines. Yet, the regulatory roles of many cytokines remain undefined at the maternal-fetal interface, including Interleukin-27 (IL-27). Here, we show that trophoblast organoids derived from human placentas constitutively express both IL-27 and its receptor, and restrict Zika virus infection through IL-27 signaling. Through bulk RNA-sequencing of trophoblast organoids in the absence and presence of IL-27 signaling, we demonstrate IL-27-mediated upregulation of antiviral genes. Finally, we show that IL-27 signaling is critical to restricting placental viral burdens and protecting against pathologic fetal outcomes during murine congenital Zika virus infection. In this work, we demonstrate a novel role for IL-27 in the placenta and establish IL-27 as an innate antiviral defense at the maternal-fetal interface during congenital viral infection.
- 19 December 2025
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Open AccessInterleukin-27 is antiviral against Zika virus at the maternal-fetal interface
Congenital viral infections can have severe consequences for pregnancy and fetal outcomes. Remarkably, the fetal-derived placenta serves as a robust barrier to infection through meticulous regulation by immune effectors and cytokines. Yet, the regulatory roles of many cytokines remain undefined at the maternal-fetal interface, including Interleukin-27 (IL-27). Here, we show that trophoblast organoids derived from human placentas constitutively express both IL-27 and its receptor, and restrict Zika virus infection through IL-27 signaling. Through bulk RNA-sequencing of trophoblast organoids in the absence and presence of IL-27 signaling, we demonstrate IL-27-mediated upregulation of antiviral genes. Finally, we show that IL-27 signaling is critical to restricting placental viral burdens and protecting against pathologic fetal outcomes during murine congenital Zika virus infection. In this work, we demonstrate a novel role for IL-27 in the placenta and establish IL-27 as an innate antiviral defense at the maternal-fetal interface during congenital viral infection.