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

作者：Sarah van Tol, Julia R. Port, Robert J. Fischer, Shane Gallogly, Trenton Bushmaker, Amanda Griffin, Jonathan E. Schulz, Aaron Carmody, Lara Myers, Daniel Crowley, Caylee Falvo, Jade C. Riopelle, Arthur Wickenhagen, Chad S. 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, Vincent J. Munster · 发表于：Nature Communications · 年份：2025 · DOI：10.1038/s41467-025-58305-4 · 被引用次数：5 · 研究领域：Viral Infections and Outbreaks Research、Viral Infections and Vectors、Hepatitis B Virus Studies

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.