Jamaican fruit bats’ competence for Ebola but not Marburg virus is driven by intrinsic differences
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.
Article Details
Authors (27)
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
College of Chemistry and Chemical Engineering
Justin Lack
Craig Martens
Sarah L. Anzick
Lon V. Kendall
Tony Schountz
Raina K. Plowright
Andrea Marzi
Vincent J. Munster