Jamaican fruit bats’ competence for Ebola but not Marburg virus is driven by intrinsic differences

Sarah van Tol, Julia R. Port, Robert J. Fischer, Shane Gallogly, Trenton Bushmaker, Amanda Griffin, Jonathan E. Schulz, Aaron Carmody, Lara Myers, Daniel E. Crowley, Caylee A. Falvo, Jade C. Riopelle, Arthur Wickenhagen, Chad Clancy, Jamie Lovaglio, Carl Shaia, Greg Saturday, Jessica Prado-Smith, Yi He, Justin Lack, Craig Martens, Sarah L. Anzick, Lon V. Kendall, Tony Schountz, Raina K. Plowright, Andrea Marzi and Vincent J. Munster ()
Additional contact information
Sarah van Tol: National Institutes of Health
Julia R. Port: National Institutes of Health
Robert J. Fischer: National Institutes of Health
Shane Gallogly: National Institutes of Health
Trenton Bushmaker: National Institutes of Health
Amanda Griffin: National Institutes of Health
Jonathan E. Schulz: National Institutes of Health
Aaron Carmody: National Institutes of Health
Lara Myers: National Institutes of Health
Daniel E. Crowley: Cornell University
Caylee A. Falvo: Cornell University
Jade C. Riopelle: National Institutes of Health
Arthur Wickenhagen: National Institutes of Health
Chad Clancy: National Institutes of Health
Jamie Lovaglio: National Institutes of Health
Carl Shaia: National Institutes of Health
Greg Saturday: National Institutes of Health
Jessica Prado-Smith: National Institutes of Health
Yi He: National Institutes of Health
Justin Lack: National Institutes of Health
Craig Martens: National Institutes of Health
Sarah L. Anzick: National Institutes of Health
Lon V. Kendall: Colorado State University
Tony Schountz: Colorado State University
Raina K. Plowright: Cornell University
Andrea Marzi: National Institutes of Health
Vincent J. Munster: National Institutes of Health

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract Ebola virus (EBOV) and Marburg virus (MARV) are zoonotic filoviruses that cause hemorrhagic fever in humans. Correlative data implicate bats as natural EBOV hosts, but neither a full-length genome nor an EBOV isolate has been found in any bats sampled. Here, we model filovirus infection in the Jamaican fruit bat (JFB), Artibeus jamaicensis, by inoculation with either EBOV or MARV through a combination of oral, intranasal, and subcutaneous routes. Infection with EBOV results in systemic virus replication and oral shedding of infectious virus. MARV replication is transient and does not shed. In vitro, JFB cells replicate EBOV more efficiently than MARV, and MARV infection induces innate antiviral responses that EBOV efficiently suppresses. Experiments using VSV pseudoparticles or replicating VSV expressing the EBOV or MARV glycoprotein demonstrate an advantage for EBOV entry and replication early, respectively, in JFB cells. Overall, this study describes filovirus species-specific phenotypes for both JFB and their cells.

Date: 2025
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DOI: 10.1038/s41467-025-58305-4

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