Urban landscapes can change virus gene flow and evolution in a fragmentation‐sensitive carnivore

Abstract

Urban expansion has widespread impacts on wildlife species globally, including the transmission and emergence of infectious diseases. However, there is almost no information about how urban landscapes shape transmission dynamics in wildlife. Using an innovative phylodynamic approach combining host and pathogen molecular data with landscape characteristics and host traits, we untangle the complex factors that drive transmission networks of feline immunodeficiency virus (FIV) in bobcats (Lynx rufus). We found that the urban landscape played a significant role in shaping FIV transmission. Even though bobcats were often trapped within the urban matrix, FIV transmission events were more likely to occur in areas with more natural habitat elements. Urban fragmentation also resulted in lower rates of pathogen evolution, possibly owing to a narrower range of host genotypes in the fragmented area. Combined, our findings show that urban landscapes can have impacts on a pathogen and its evolution in a carnivore living in one of the most fragmented and urban systems in North America. The analytical approach used here can be broadly applied to other host-pathogen systems, including humans.

Viruses as indicators of contemporary host dispersal and phylogeography: an example of feline immunodeficiency virus (FIVPle) in free‐ranging African lion (Panthera leo)

“…Whereas FIV failed to detect phylogeographic patterns in a previous study which focused on bobcats living in an urban landscape (Lee et al ., ), our current findings are supported by a recent study undertaken by Fountain‐Jones et al . () which showed FIV structure in bobcats. Patterns in the spatial distribution of FIV Ple subtypes across the landscape have been suggested previously at the larger continental scale (Antunes et al ., ).…”

“…The pol‐ RT region was selected as it has been widely used to investigate FIV diversity both within and between species (Troyer et al ., , ; Franklin et al ., ; Lee et al ., ). More specifically, it has also been used previously to evaluate phylogeographic structure in 105 bobcats (solitary species; Lee et al ., ; Fountain‐Jones et al ., ) and more recently in 216 lions from the Serengeti (social species; Fountain‐Jones et al ., ). These primers were selected as they preferentially amplify one subtype in co‐infected individuals and it has been proposed that their amplification success may be linked to viral load (Troyer et al ., ).…”

Pathogens in space: Advancing understanding of pathogen dynamics and disease ecology through landscape genetics

“…Further, viruses are prominent emerging pathogens and have relatively small genomes, aiding whole genome‐analysis. Landscape effects on viral transmission are typically studied using phylogenetic approaches (Fountain‐Jones, Craft et al., ; Joannon, Lavigne, Lecoq, & Desbiez, ; Streicker et al., ; Young et al., ). To date, pathogens with larger and more slowly mutating genomes, such as protozoans (Carrel et al., ; Lo et al., ) and fungi (Brar et al., ; Rieux, De Bellaire, Zapater, Ravigne, & Carlier, ), have been studied using population genetics‐based methods with highly variable microsatellite and SNP loci.…”

“…These characteristics may be less problematic for agricultural populations where morbidity or mortality can be identified and samples collected immediately, but inevitably leave “breaks” in the inferred chain of transmission among wild populations. While complete sampling of wild populations is rarely possible in any case, obtaining adequate sample sizes is easier for apathogenic or low‐pathogenicity agents that form chronic infections and may be sampled at any time postinfection (e.g., feline immunodeficiency virus; Biek et al., ; Lee et al., ; Fountain‐Jones, Craft et al., ). Landscape genetic study of such “model” infectious agents may be used to target specific ecological questions and provide insights into how similarly transmitted agents with higher pathogenicity might spread in the event of an outbreak.…”

Population genetics of fruit bat reservoir informs the dynamics, distribution and diversity of Nipah virus

“…The structure and connectivity of wildlife host populations may influence zoonotic disease dynamics, evolution and spillover risk to people (Biek & Real, ; Cross, Lloyd‐Smith, Johnson, & Getz, ). A better understanding of host population genetic structure will therefore likely improve models of viral circulation dynamics (Goldsmith et al, ; Gryseels et al, ; Guivier et al, ; Rodríguez‐Nevado, Lam, Holmes, & Pagán, ; Streicker et al, ; Wilder, Kunz, & Sorenson, ), but see Fountain‐Jones et al () and Lee et al (). Evolutionary dynamics may also be important in zoonotic emergence, and structuring of host populations has been shown to influence the evolution of pathogen virulence and infectivity (Boots, Hudson, & Sasaki, ; Boots & Mealor, ).…”