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.

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Publication Details

Journal
Nature Communications
Published
2025-12-19
DOI
https://doi.org/10.1038/s41467-025-67378-0
Citations
1
Primary Topic
Psoriasis: Treatment and Pathogenesis
Type
article
Field-Weighted Citation Impact
0.80

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article

Interleukin-27 is antiviral against Zika virus at the maternal-fetal interface

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1 citations
Nature Communications
Psoriasis: Treatment and Pathogenesis
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article

Interleukin-27 is antiviral against Zika virus at the maternal-fetal interface

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article en
1 citations

Abstract

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.

Nature CommunicationsVol. 17(1)
Hospital of the University of Pennsylvania (US), University of Pennsylvania (US)
Children's Hospital of Philadelphia, University of Pennsylvania, Washington University in St. Louis
Openalex Percentile: Top 20%
Psoriasis: Treatment and Pathogenesis
0.80
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