Prenatal exposure to Zika virus shapes offspring neutrophil function in a sex-specific manner

Jiahui Ding (), Anna Hu, Annie Thy Nguyen, Grace M. Swanson, Aditi Singh, Nicholas Adzibolosu, Diana Manchorova, Elizabeth Findeis, Anthony Maxwell, Yuan He, Marta Rodriguez Garcia and Gil Mor
Additional contact information
Jiahui Ding: Wayne State University
Anna Hu: Wayne State University
Annie Thy Nguyen: Wayne State University
Grace M. Swanson: Wayne State University
Aditi Singh: Wayne State University
Nicholas Adzibolosu: Wayne State University
Diana Manchorova: Wayne State University
Elizabeth Findeis: Wayne State University
Anthony Maxwell: Wayne State University
Yuan He: Wayne State University
Marta Rodriguez Garcia: Wayne State University
Gil Mor: Wayne State University

Nature Communications, 2025, vol. 16, issue 1, 1-19

Abstract: Abstract Maternal viral infection during pregnancy can have lasting consequences on offspring immune development. Zika virus (ZIKV) is known to trigger maternal immune activation (MIA), yet its impact on fetal and postnatal innate immunity remains poorly understood. Here, we investigate how prenatal exposure to ZIKV influences offspring neutrophil function using a murine model of maternal infection. We identify a sex-dimorphic placental response to ZIKV and observed hyperinflammation in ZIKV-exposed male offspring following LPS challenge. Functional assays reveal impaired reactive oxygen species production and defective neutrophil extracellular trap formation in neutrophils from ZIKV-exposed offspring. Furthermore, we identify A20 as a key sex-dimorphic regulator of neutrophil activation and survival. Here, we show that maternal viral infection during pregnancy programs long-term offspring immunity in a sex-specific manner, providing insights into the developmental origins of differential susceptibility to infections and inflammatory diseases later in life.

Date: 2025
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DOI: 10.1038/s41467-025-63941-x

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