Biology subjects
Publications and source records attributed to Falvo, C..
We explore the role of Australian black flying foxes (Pteropus alecto) as reservoir hosts of potentially zoonotic Borrelia bacteria. Across six sites, 2% of 840 bats were infected with one of two novel Borrelia haplotypes. Phylogenetic reconstruction indicated these infections are distinct from Lyme or relapsing fever clades.
Ebola virus (EBOV) and Marburg virus (MARV) are zoonotic filoviruses that cause hemorrhagic fever in humans. Bat species in both Chiropteran suborders host filoviruses, suggesting that bats may have coevolved with this viral family. 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 modelled filovirus infection in the Jamaican fruit bat (JFB), Artibeus jamaicensis. Bats were inoculated with either EBOV or MARV through a combination of oral, intranasal, and subcutaneous routes. EBOV-infected bats supported systemic virus replication and shed infectious virus orally. In contrast, MARV replicated only transiently and was not shed. In vitro, JFB cells replicate EBOV more efficiently than MARV, and MARV infection induced innate antiviral responses that EBOV efficiently suppressed. Experiments using VSV pseudoparticles or replicating VSV expressing the EBOV or MARV glycoprotein demonstrated 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.
Changes in the quality and quantity of food resources can affect individuals health, the way they control infections and consequently the likelihood of onward transmission of pathogens. Dietary shifts have been proposed as one of the factors driving spillovers of zoonotic viruses from bats through a bridging host to humans. While there is a general understanding of the relationship between nutrition and infection in model systems, how diet affects pathogen shedding and the risk of spillover from bats is lacking. We used a data-driven mathematical modeling approach to disentangle the relation between diet, immunity, and viral shedding of Jamaican fruit bats infected with H18N11 and fed different dietary regimes. Model selection indicates that the synergistic interaction between the metabolite citrulline and the cytokine TNF controls viral shedding in a diet-dependent manner. Bats on a sub-optimal fat diet are more successful in terminating shedding than bats on an optimal or sub-optimal sugar diet. However, when bat foraging behavior is considered, bats on the optimal diet show a lower spillover hazard, probably because of a feeding behavior less conducive to transmission. This study provides novel insights into the diet-driven mechanisms of viral shedding and how they can potentially contribute to spillover events.
Land-use change may drive viral spillover from bats into humans, partly through dietary shifts caused by decreased availability of native foods and increased availability of cultivated foods. We manipulated diets of Jamaican fruit bats to investigate whether diet influences shedding of a virus they naturally host. To reflect dietary changes experienced by wild bats during periods of nutritional stress, bats were fed either standard or putative suboptimal diets which were deprived of protein (suboptimal-sugar) and/or supplemented with fat (suboptimal-fat). Upon H18N11 influenza A-virus infection, bats fed the suboptimal-sugar diet shed the most viral RNA for the longest period, but bats fed the suboptimal-fat diet shed the least viral RNA for the shortest period. Unlike mice and humans, bats fed the suboptimal-fat diet displayed higher pre-infection levels of metabolic markers associated with gut health. Diet-driven heterogeneity in viral shedding may influence population-level viral dynamics in wild bats and alter risk of shedding and spillover to humans.