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Infectious diseases are a major threat for biodiversity conservation and can exert strong influence on wildlife population dynamics. Understanding the mechanisms driving infection rates and epidemic outcomes requires empirical data on the evolutionary trajectory of pathogens and host selective processes. Phylodynamics is a robust framework to understand the interaction of pathogen evolutionary processes with epidemiological dynamics, providing a powerful tool to evaluate disease control strategies. Tasmanian devils have been threatened by a fatal transmissible cancer, devil facial tumour disease (DFTD), for more than two decades. Here we employ a phylodynamic approach using tumour mitochondrial genomes to assess the role of tumour genetic diversity in epidemiological and population dynamics in a devil population subject to 12 years of intensive monitoring, since the beginning of the epidemic outbreak. DFTD molecular clock estimates of disease introduction mirrored observed estimates in the field, and DFTD genetic diversity was positively correlated with estimates of devil population size. However, prevalence and force of infection were the lowest when devil population size and tumour genetic diversity was the highest. This could be due to either differential virulence or transmissibility in tumour lineages or the development of host defence strategies against infection. Our results support the view that evolutionary processes and epidemiological trade‐offs can drive host‐pathogen coexistence, even when disease‐induced mortality is extremely high. We highlight the importance of integrating pathogen and population evolutionary interactions to better understand long‐term epidemic dynamics and evaluating disease control strategies.

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.

Functional traits mediate species' responses to, and roles within, their environment and are constrained by evolutionary history. While we have a strong understanding of trait evolution for macro‐taxa such as birds and mammals, our understanding of invertebrates is comparatively limited. Here, we address this gap in North American beetles with a sample of ground beetles (Carabidae), leveraging a large‐scale collection and digitization effort by the National Ecological Observatory Network (NEON). For 154 ground beetle species, we measured seven morphological traits, which we placed into a recently developed effect–response framework that characterizes traits by how they predict species' effects on their ecosystems or responses to environmental stressors. We then used cytochrome oxidase 1 sequences from the same specimens to generate a phylogeny and tested the evolutionary tempo and mode of the traits. We found strong phylogenetic signal in, and correlations among, ground beetle morphological traits. These results indicate that, for these species, beetle body shape trait evolution is constrained, and phylogenetic inertia is a stronger driver of beetle traits than (recent) environmental responses. Strong correlations among effect and response traits suggest that future environmental drivers are likely to affect both ecological composition and functioning in these beetles.

We introduce a new R package “MrIML” (“Mister iml”; Multi‐response Interpretable Machine Learning). MrIML provides a powerful and interpretable framework that enables users to harness recent advances in machine learning to quantify multilocus genomic relationships, to identify loci of interest for future landscape genetics studies, and to gain new insights into adaptation across environmental gradients. Relationships between genetic variation and environment are often nonlinear and interactive; these characteristics have been challenging to address using traditional landscape genetic approaches. Our package helps capture this complexity and offers functions that fit and interpret a wide range of highly flexible models that are routinely used for single‐locus landscape genetics studies but are rarely extended to estimate response functions for multiple loci. To demonstrate the package's broad functionality, we test its ability to recover landscape relationships from simulated genomic data. We also apply the package to two empirical case studies. In the first, we model genetic variation of North American balsam poplar (Populus balsamifera, Salicaceae) populations across environmental gradients. In the second case study, we recover the landscape and host drivers of feline immunodeficiency virus genetic variation in bobcats (Lynx rufus). The ability to model thousands of loci collectively and compare models from linear regression to extreme gradient boosting, within the same analytical framework, has the potential to be transformative. The MrIML framework is also extendable and not limited to modelling genetic variation; for example, it can quantify the environmental drivers of microbiomes and coinfection dynamics.

Predicting infectious disease dynamics is a central challenge in disease ecology. Models that can assess which individuals are most at risk of being exposed to a pathogen not only provide valuable insights into disease transmission and dynamics but can also guide management interventions. Constructing such models for wild animal populations, however, is particularly challenging; often only serological data are available on a subset of individuals and nonlinear relationships between variables are common.

The spatial organization of a population can influence the spread of information, behaviour and pathogens. Group territory size and territory overlap and components of spatial organization, provide key information as these metrics may be indicators of habitat quality, resource dispersion, contact rates and environmental risk (e.g. indirectly transmitted pathogens). Furthermore, sociality and behaviour can also shape space use, and subsequently, how space use and habitat quality together impact demography.

Pathogens are embedded in a complex network of microparasites that can collectively or individually alter disease dynamics and outcomes. Endemic pathogens that infect an individual in the first years of life, for example, can either facilitate or compete with subsequent pathogens thereby exacerbating or ameliorating morbidity and mortality. Pathogen associations are ubiquitous but poorly understood, particularly in wild populations. We report here on 10 years of serological and molecular data in African lions, leveraging comprehensive demographic and behavioural data to test if endemic pathogens shape subsequent infection by epidemic pathogens. We combine network and community ecology approaches to assess broad network structure and characterise associations between pathogens across spatial and temporal scales. We found significant non‐random structure in the lion‐pathogen co‐occurrence network and identified both positive and negative associations between endemic and epidemic pathogens. Our results provide novel insights on the complex associations underlying pathogen co‐occurrence networks.