Biology subjects

Sweeny, A.

Publications and source records attributed to Sweeny, A..

4 recordsLinked to original sources

bioRxiv2026

Wild wood mouse gut microbiota are influenced by captivity and cross-fostering

Background Wild and laboratory animals harbour profoundly different gut microbiota, but how microbiomes shift between these states, and the relative roles of captivity, microbial history, and host identity in shaping that shift, remain unclear. Here, we developed a unique wood mouse (Apodemus sylvaticus) system comprising free-living mice (Wild:As), a wild-derived colony maintained in captivity for over a decade (Wild-like:As), and a second colony that we generated from the Wild-like:As mice by caesarean rederivation and cross-fostering to laboratory Mus musculus (Lab-like:As). We compared these three Apodemus cohorts with conventional laboratory Mus musculus (Lab:Mm) to ask how microbial diversity, community composition, and functional potential vary across a spectrum of wild-to-laboratory conditions. Results We found that alpha diversity varied substantially among cohorts but showed no consistent wild-to-laboratory trend: Shannon diversity was higher in Lab:Mm and Lab-like:As than in Wild:As and Wild-like:As mice, whereas phylogenetic diversity was similarly high in both the Wild:As and Lab:Mm groups. Community composition more closely reflected cohort histories. Despite over a decade in captivity, Wild-like:As mice remained most similar to Wild:As conspecifics, whereas Lab-like:As mice shifted strongly away from Wild-like:As and toward, but remained distinct from, Lab:Mm mice. The clearest wild-to-laboratory pattern emerged in microbiome consistency: core ASVs (present in [≥]90% of individuals) increased from 9 in Wild:As to 46 in Wild-like:As, 72 in Lab-like:As, and 138 in Lab:Mm mice. Predicted functional potential revealed a further distinction between taxonomic and functional patterns: Wild:As and Wild-like:As microbiomes did not differ significantly, whereas Lab-like:As shifted toward the Lab:Mm state despite remaining taxonomically distinct. Conclusions Together, these results show that laboratory-associated microbiomes do not emerge through simple loss of wild microbial diversity, but through broader reorganisation of community composition, consistency, and predicted functional potential reflecting microbial history and host context. The persistent Wild-like and Lab-like microbiome states within Apodemus provide a powerful experimental system for future timely work testing how microbiome history influences host physiology, resilience, and responses to environmental challenges.

microbiology↗

bioRxiv2025

Environmental drivers of low vaccine responsiveness in a lab-to-wild rodent model

Vaccination is the most effective way to prevent infectious diseases and safeguard public health. Yet, most new vaccines fail in late clinical trials, and even estab-lished ones often underperform in populations apart from those in which they were initially tested. This can lead to reduced vaccine responsiveness, breakthrough infections, and prevent or delay herd immunity. While the causes of vaccine hypore-sponsiveness remain difficult to identify, quantify, and therefore address, numerous reports indicate a predominant role of environmental factors. This has notably been demonstrated by a reduction in the immunogenicity and efficacy of various vaccines when transitioning from urban to rural human populations. Here, we tested whether and, if so, how the environment can cause vaccine hyporesponsive-ness. We hypothesised that if the leading causes of vaccine hyporesponsiveness were environmental, then the reduced efficacy would be exacerbated when indi-viduals are under nutritional stress; specifically predicting that high quality diet supplementation would increase vaccine responsiveness. Finally, we predicted that parasitic helminth infection, which are more common in rural populations, would degrade vaccine responsiveness, e.g. due to their ability to suppress host immunity, and that anthelmintic treatment could rescue vaccine responsiveness in infected individuals. To test these hypotheses, we coupled lab and field experiments with structural causal modelling, and measured antibody responses of paired conspecific cohorts of laboratory-reared and wild wood mice (Apodemus sylvaticus) to a single or two doses of diphtheria toxoid vaccine formulated with alum; with and without diet supplementation. We found that vaccine-specific IgG1 antibodies were [~]47% lower in the wild wood mice compared to the laboratory reared population. We also demonstrate that, across both habitats (wild and lab), substantial variation in vaccine responsiveness was caused by diet. However, contrary to our predictions, this high quality dietary supplementation resulted in lower vaccine responsiveness. Further, once the effects of habitat, diet, and sex were adjusted for, increasing hel-minth infection burdens negatively affected vaccine-specific antibody production. Using counterfactual modelling, we show that targeting anthelmintic treatment at heavily infected individuals would have improved their vaccine responsiveness by 2 to 4-fold. Our results indicate that the wild environment and access to a high-quality diet play a dramatic role in shaping the immune systems response to immunisation. Further, we show that laboratory settings, even when using a genetic diverse, non-traditional model, may systematically overestimate vaccine performance by failing to capture natural environmental variability. Our study provides a robust, causally explicit modelling approach to disentangle and quantify the complex factors that drive vaccine responsiveness in focal populations. This framework offers a path-way for predicting vaccine performance across diverse populations and identifying targeted interventions to enhance immunisation outcomes in real-world settings.

systems biology↗

bioRxiv2022

Exploring the mosquito-arbovirus network: a survey of vector competence experiments

Arboviruses receive heightened research attention during major outbreaks, or when they cause unusual or severe clinical disease, but are otherwise under-characterized. Global change is also accelerating the emergence and spread of arboviral diseases, leading to time sensitive questions about potential interactions between viruses and novel vectors. Vector competence experiments help determine the susceptibility of certain arthropods to a given arbovirus, but these experiments are often conducted in real-time during outbreaks, rather than with preparedness in mind. We conducted a systematic review of reported mosquito-arbovirus competence experiments, screening 570 abstracts to arrive at 265 studies testing in vivo arboviral competence. We found that over 90% of potential mosquito-virus combinations are untested in experimental settings, and that entire regions and their corresponding vectors and viruses are undersampled. These knowledge gaps stymie outbreak response, and limit attempts to both build and validate predictive models of the vector-virus network.

ecology↗

bioRxiv2020

Fine-scale spatial patterns of wildlife disease are common and understudied

O_LIAll parasites are heterogeneous in space, yet little is known about the prevalence and scale of this spatial variation, particularly in wild animal systems. To address this question, we sought to identify and examine spatial dependence of wildlife disease across a wide range of systems. C_LIO_LIConducting a broad literature search, we collated 31 such datasets featuring 89 replicates and 71 unique host-parasite combinations, only 51% of which had previously been used to test spatial hypotheses. We analysed these datasets for spatial dependence within a standardised modelling framework using Bayesian linear models, and we then meta-analysed the results to identify generalised determinants of the scale and magnitude of spatial autocorrelation. C_LIO_LIWe detected spatial autocorrelation in 48/89 model replicates (54%) across 21/31 datasets (68%), spread across parasites of all groups. Even some very small study areas (under 0.01km2) exhibited substantial spatial variation. C_LIO_LIDespite the common manifestation of spatial variation, our meta-analysis was unable to identify host-, parasite-, or sampling-level determinants of this heterogeneity across systems. Parasites of all transmission modes had easily detectable spatial patterns, implying that structured contact networks and susceptibility effects are potentially as important in spatially structuring disease as are environmental drivers of transmission efficiency. C_LIO_LIOur findings demonstrate that fine-scale spatial patterns of infection manifest frequently and across a range of wild animal systems, and many studies are able to investigate them whether or not the original aim of the study was to examine spatially varying processes. Given the widespread nature of these findings, studies should more frequently record and analyse spatial data, facilitating development and testing of spatial hypotheses in disease ecology. Ultimately, this may pave the way for an a priori predictive framework for spatial variation in novel host-parasite systems. C_LI

ecology↗