Urban expansion can fundamentally alter wildlife movement and gene flow, but how urbanization alters pathogen spread is poorly understood. Here, we combine high resolution host and viral genomic data with landscape variables to examine the context of viral spread in puma (Puma concolor) from two contrasting regions: one bounded by the wildland urban interface (WUI) and one unbounded with minimal anthropogenic development (UB). We found landscape variables and host gene flow explained significant amounts of variation of feline immunodeficiency virus (FIV) spread in the WUI, but not in the unbounded region. The most important predictors of viral spread also differed; host spatial proximity, host relatedness, and mountain ranges played a role in FIV spread in the WUI, whereas roads might have facilitated viral spread in the unbounded region. Our research demonstrates how anthropogenic landscapes can alter pathogen spread, providing a more nuanced understanding of host-pathogen relationships to inform disease ecology in free-ranging species.
Bibliographical noteFunding Information:
This project was funded by a National Science Foundation Ecology of Infectious Diseases research program grants (DEB 1413925). M.C. was funded by the University of Minnesota’s Office of the Vice President for Research and Academic Health Center Seed Grant. G.B. acknowledges support from the Interne Fondsen KU Leuven/Internal Funds KU Leuven under grant agreement C14/18/094, and the Research Foundation—Flanders (“Fonds voor Wetenschappelijk Onderzoek—Vlaanderen,” G0E1420N). We thank Bill Peterman for his advice on the resistanceGA pipeline.
© 2021, The Author(s).