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Developing and Characterizing a Murine Model of In Utero Transmission of Ebola Virus
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Developing and Characterizing a Murine Model of In Utero Transmission of Ebola Virus

Hanora Van Ert, Corey W. Henderson, Brian J. Smith, Paige T. Donovan, Ethan Kardin, Emma Eubank, Maryam Fakhimi, Matthew Liebermann, Kelly N. Messingham, Mark K. Santillan, …
bioRxiv
Cold Spring Harbor Laboratory, 1.1
08/05/2026
DOI: 10.64898/2026.08.04.742335
PMID: 42620007
url
https://doi.org/10.64898/2026.08.04.742335View
Preprint (Author's original) This preprint has not been evaluated by subject experts through peer review. Preprints may undergo extensive changes and/or become peer-reviewed journal articles. Open Access

Abstract

Ebola virus (EBOV) disease (EVD) is a hemorrhagic disease caused by EBOV infection. EVD outcomes in pregnant women are similar to non-pregnant women however, EVD is associated with negative fetal outcomes in ∼99% of cases. There is a critical need for a tractable small animal model to study maternal/fetal transmission of EBOV. We utilized interferon α/β receptor knock out mice infected and authentic EBOV or the model virus, recombinant vesicular stomatitis virus encoding EBOV glycoprotein (rVSV/EBOV). Infection with either virus during late pregnancy resulted in placental infection and vertical transmission to the fetus within 2-3 days. Robust levels of maternal and fetal proinflammatory cytokines were evident by day 5 after EBOV infection. Within the placenta, trophoblasts and endothelial cells were viral antigen positive. Elimination of the endosomal receptor NPC1 in junctional zone trophoblasts reduced placental infection and virus transmission to the fetus. These studies establish an infectious model that provides EBOV trafficking and pathogenesis insights during pregnancy. This model provides key insights into how viral trafficking and maternal immune responses drive adverse fetal outcomes during gestational Ebola virus infection.
Microbiology

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