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

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.

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Publication Details

Journal
Nature Communications
Published
2025-03-25
DOI
https://doi.org/10.1038/s41467-025-58305-4
Citations
3
Primary Topic
Viral Infections and Outbreaks Research
Type
article
Field-Weighted Citation Impact
4.19

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article

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

Raina K. Plowright, Lara Myers, Lon V. Kendall, Tony Schountz et al.
3 citations
Nature Communications
Viral Infections and Outbreaks Research
4.19
article

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

Raina K. Plowright, Lara Myers, Lon V. Kendall, Tony Schountz, Carl Shaia, Julia Rebecca Port, Vincent J. Munster, Robert J. Fischer, Greg Saturday, Amanda M. Griffin, Chad S. Clancy, Jonathan E. Schulz, Justin Lack, Daniel Crowley, Jade C. Riopelle, Craig Martens, Jamie Lovaglio, Sarah van Tol, Andrea Marzi, Trenton Bushmaker, Aaron Carmody, Arthur Wickenhagen, Sarah L. Anzick, Caylee Falvo, Jessica Prado-Smith, Yi He, Shane Gallogly
article en
3 citations

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.

Nature CommunicationsVol. 16(1)
National Institutes of Health (US), Cornell University (US), Helmholtz Centre for Infection Research (DE), National Institute of Allergy and Infectious Diseases (US), National Institutes of Health Clinical Center (US), Colorado State University (US)
Division of Intramural Research, National Institute of Allergy and Infectious Diseases
Openalex Percentile: Top 7%
Viral Infections and Outbreaks Research
4.19
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