Much of the basic ecology of Ebolavirus remains unresolved despite accumulating disease outbreaks, viral strains and evidence of animal hosts. Because human Ebolavirus epidemics have been linked to contact with wild mammals other than bats, traits shared by species that have been infected by Ebolavirus and their phylogenetic distribution could suggest ecological mechanisms contributing to human Ebolavirus spillovers. We compiled data on Ebolavirus exposure in mammals and corresponding data on life-history traits, movement, and diet, and used boosted regression trees (BRT) to identify predictors of exposure and infection for 119 species (hereafter hosts). Mapping the phylogenetic distribution of presumptive Ebolavirus hosts reveals that they are scattered across several distinct mammal clades, but concentrated among Old World fruit bats, primates and artiodactyls. While sampling effort was the most important predictor, explaining nearly as much of the variation among hosts as traits, BRT models distinguished hosts from all other species with greater than 97% accuracy, and revealed probable Ebolavirus hosts as large-bodied, frugivorous, and with slow life histories. Provisionally, results suggest that some insectivorous bat genera, Old World monkeys and forest antelopes should receive priority in Ebolavirus survey efforts.
© 2019 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.
Boosted regression trees, Comparative analysis, Ebola, Frugivory, Host
Schmidt, John Paul, Sean Maher, John M. Drake, Tao Huang, Maxwell J. Farrell, and Barbara A. Han. "Ecological indicators of mammal exposure to Ebolavirus." Philosophical Transactions of the Royal Society B 374, no. 1782 (2019): 20180337.
Philosophical Transactions of the Royal Society B: Biological Sciences
This article is part of the theme issue ‘Dynamic and integrative approaches to understanding pathogen spillover’.