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Suicide results from complex interactions between biological, psychological, and socioeconomic factors. At the population level, the study of suicide rates and their environmental and social determinants allows us to disentangle some of these complexities and provides support for policy design and preventive actions. In this study we aim to evaluate the associations between environmental and socioeconomic factors and demographically stratified suicide rates on large temporal and spatial scales. Our dataset contains information about yearly suicides rates by sex and age from 2000 through 2017 along a 4000 km latitudinal gradient. We used zero-inflated negative binomial models to evaluate the spatio-temporal influence of each environmental and socioeconomic variable on suicide rates at each sex/age combination. Overall, we found differential patterns of associations between suicide rates and explanatory variables by age and sex. Suicide rates in men increases in middle and high latitude regions and intermediate age classes. For adolescent and adult women, we found a similar pattern with an increase in suicide rates at middle and high latitudes. Sex differences measured by the male/female suicide ratio shows a marked increase with age. We found that cloudiness has a positive effect on suicide rates in both men and women 24 years old or younger. Regional poverty shows a major impact on men in age classes above 35 years old, an effect that was absent in women. Alcohol and marijuana consumption showed no significant effect sizes. Our findings support high spatio-temporal variability in suicide rates in interaction with extrinsic factors. Several strong differential impacts of environmental and socioeconomic variables on suicide rates depending on sex and age were detected. These results suggest that the design of public policies and interventions to reduce suicide prevalence need to consider the local social and environmental contexts of target populations.

The iconic Tasmanian devil (Sarcophilus harrisii) is endangered due to the transmissible cancer Devil Facial Tumour Disease (DFTD), of which there are two genetically independent subtypes (DFT1 and DFT2). While DFT1 and DFT2 can be differentially diagnosed using tumour biopsies, there is an urgent need to develop less-invasive biomarkers that can detect DFTD and distinguish between subtypes. Extracellular vesicles (EVs), the nano-sized membrane-enclosed vesicles present in most biofluids, represent a valuable resource for biomarker discovery. Here, we characterized the proteome of EVs from cultured DFTD cells using data-independent acquisition–mass spectrometry and an in-house spectral library of > 1500 proteins. EVs from both DFT1 and DFT2 cell lines expressed higher levels of proteins associated with focal adhesion functions. Furthermore, hallmark proteins of epithelial–mesenchymal transition were enriched in DFT2 EVs relative to DFT1 EVs. These findings were validated in EVs derived from serum samples, revealing that the mesenchymal marker tenascin-C was also enriched in EVs derived from the serum of devils infected with DFT2 relative to those infected with DFT1 and healthy controls. This first EV-based investigation of DFTD increases our understanding of the cancers’ EVs and their possible involvement in DFTD progression, such as metastasis. Finally, we demonstrated the potential of EVs to differentiate between DFT1 and DFT2, highlighting their potential use as less-invasive liquid biopsies for the Tasmanian devil.

The COVID‐19 pandemic has highlighted the importance of efficient sampling strategies and statistical methods for monitoring infection prevalence, both in humans and in reservoir hosts. Pooled testing can be an efficient tool for learning pathogen prevalence in a population. Typically, pooled testing requires a second‐phase retesting procedure to identify infected individuals, but when the goal is solely to learn prevalence in a population, such as a reservoir host, there are more efficient methods for allocating the second‐phase samples.To estimate pathogen prevalence in a population, this manuscript presents an approach for data fusion with two‐phased testing of pooled samples that allows more efficient estimation of prevalence with less samples than traditional methods. The first phase uses pooled samples to estimate the population prevalence and inform efficient strategies for the second phase. To combine information from both phases, we introduce a Bayesian data fusion procedure that combines pooled samples with individual samples for joint inferences about the population prevalence.Data fusion procedures result in more efficient estimation of prevalence than traditional procedures that only use individual samples or a single phase of pooled sampling.The manuscript presents guidance on implementing the first‐phase and second‐phase sampling plans using data fusion. Such methods can be used to assess the risk of pathogen spillover from reservoir hosts to humans, or to track pathogens such as SARS‐CoV‐2 in populations., Pooled testing is a common procedure for efficient sampling to determine population prevalence and identify positive individuals. When the goal is to learn population prevalence, without regard for identifying positive individuals, data integration results in more precise estimates than retesting individuals in positive pools.

Devil facial tumor disease (DFTD) is a transmissible cancer affecting Tasmanian devils Sarcophilus harrisii. The disease has caused severe population declines and is associated with demographic and behavioral changes, including earlier breeding, younger age structures, and reduced dispersal and social interactions. Devils are generally solitary, but social encounters are commonplace when feeding upon large carcasses. DFTD tumors can disfigure the jaw and mouth and so diseased individuals might alter their diets to enable ingestion of alternative foods, to avoid conspecific interactions, or to reduce competition. Using stable isotope analysis (δ13C and δ15N) of whiskers, we tested whether DFTD progression, measured as tumor volume, affected the isotope ratios and isotopic niches of 94 infected Tasmanian devils from six sites in Tasmania, comprising four eucalypt plantations, an area of smallholdings and a national park. Then, using tissue from 10 devils sampled before and after detection of tumors and 8 devils where no tumors were detected, we examined whether mean and standard deviation of δ13C and δ15N of the same individuals changed between healthy and diseased states. δ13C and δ15N values were generally not related to tumor volume in infected devils, though at one site, Freycinet National Park, δ15N values increased significantly as tumor volume increased. Infection with DFTD was not associated with significant changes in the mean or standard deviation of δ13C and δ15N values in individual devils sampled before and after detection of tumors. Our analysis suggests that devils tend to maintain their isotopic niche in the face of DFTD infection and progression, except where ecological conditions facilitate a shift in diets and feeding behaviors, demonstrating that ecological context, alongside disease severity, can modulate the behavioral responses of Tasmanian devils to DFTD.

Genetic structure in host species is often used to predict disease spread. However, host and pathogen genetic variation may be incongruent. Understanding landscape factors that have either concordant or divergent influence on host and pathogen genetic structure is crucial for wildlife disease management. Devil facial tumour disease (DFTD) was first observed in 1996 and has spread throughout almost the entire Tasmanian devil geographic range, causing dramatic population declines. Whereas DFTD is predominantly spread via biting among adults, devils typically disperse as juveniles, which experience low DFTD prevalence. Thus, we predicted little association between devil and tumour population structure and that environmental factors influencing gene flow differ between devils and tumours. We employed a comparative landscape genetics framework to test the influence of environmental factors on patterns of isolation by resistance (IBR) and isolation by environment (IBE) in devils and DFTD. Although we found evidence for broad-scale costructuring between devils and tumours, we found no relationship between host and tumour individual genetic distances. Further, the factors driving the spatial distribution of genetic variation differed for each. Devils exhibited a strong IBR pattern driven by major roads, with no evidence of IBE. By contrast, tumours showed little evidence for IBR and a weak IBE pattern with respect to elevation in one of two tumour clusters we identify herein. Our results warrant caution when inferring pathogen spread using host population genetic structure and suggest that reliance on environmental barriers to host connectivity may be ineffective for managing the spread of wildlife diseases. Our findings demonstrate the utility of comparative landscape genetics for identifying differential factors driving host dispersal and pathogen transmission.

Spontaneous tumor regression has been documented in a small proportion of human cancer patients, but the specific mechanisms underlying tumor regression without treatment are not well understood. Tasmanian devils are threatened with extinction from a transmissible cancer due to universal susceptibility and a near 100% case fatality rate. In over 10,000 cases

Age‐related changes in diet have implications for competitive interactions and for predator–prey dynamics, affecting individuals and groups at different life stages. To quantify patterns of variation and ontogenetic change in the diets of Tasmanian devils Sarcophilus harrisii, a threatened marsupial carnivore, we analyzed variation in the stable isotope composition of whisker tissue samples taken from 91 individual devils from Wilmot, Tasmania from December 2014 to February 2017. Both δ13C and δ15N decreased with increasing age in weaned Tasmanian devils, indicating that as they age devils rely less on small mammals and birds, and more on large herbivores. Devils, By using stable isotope analysis of whiskers, we quantify variation in the isotopic trophic niches of Tasmanian devils as they age. We highlight changes in the isotopic composition and variation of devil whiskers with increasing age, reflecting the effect of weaning in early life, and a likely shift from a diverse subadult diet of small mammals, birds and invertebrates through to larger herbivores in adulthood.

In the past two decades, three coronaviruses with ancestral origins in bats have emerged and caused widespread outbreaks in humans, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since the first SARS epidemic in 2002–2003, the appreciation of bats as key hosts of zoonotic coronaviruses has advanced rapidly. More than 4,000 coronavirus sequences from 14 bat families have been identified, yet the true diversity of bat coronaviruses is probably much greater. Given that bats are the likely evolutionary source for several human coronaviruses, including strains that cause mild upper respiratory tract disease, their role in historic and future pandemics requires ongoing investigation. We review and integrate information on bat–coronavirus interactions at the molecular, tissue, host and population levels. We identify critical gaps in knowledge of bat coronaviruses, which relate to spillover and pandemic risk, including the pathways to zoonotic spillover, the infection dynamics within bat reservoir hosts, the role of prior adaptation in intermediate hosts for zoonotic transmission and the viral genotypes or traits that predict zoonotic capacity and pandemic potential. Filling these knowledge gaps may help prevent the next pandemic., Bats harbour a multitude of coronaviruses and owing to their diversity and wide distribution are prime reservoir hosts of emerging viruses. Ruiz-Aravena, McKee and colleagues analyse the currently available information on bat coronaviruses and discuss their role in recent and potential future spillovers.

Background Transmissible cancers lie at the intersection of oncology and infectious disease, two traditionally divergent fields for which gene expression studies are particularly useful for identifying the molecular basis of phenotypic variation. In oncology, transcriptomics studies, which characterize the expression of thousands of genes, have identified processes leading to heterogeneity in cancer phenotypes and individual prognoses. More generally, transcriptomics studies of infectious diseases characterize interactions between host, pathogen, and environment to better predict population-level outcomes. Tasmanian devils have been impacted dramatically by a transmissible cancer (devil facial tumor disease; DFTD) that has led to widespread population declines. Despite initial predictions of extinction, populations have persisted at low levels, due in part to heterogeneity in host responses, particularly between sexes. However, the processes underlying this variation remain unknown. Results We sequenced transcriptomes from healthy and DFTD-infected devils, as well as DFTD tumors, to characterize host responses to DFTD infection, identify differing host-tumor molecular interactions between sexes, and investigate the extent to which tumor gene expression varies among host populations. We found minimal variation in gene expression of devil lip tissues, either with respect to DFTD infection status or sex. However, 4088 genes were differentially expressed in tumors among our sampling localities. Pathways that were up- or downregulated in DFTD tumors relative to normal tissues exhibited the same patterns of expression with greater intensity in tumors from localities that experienced DFTD for longer. No mRNA sequence variants were associated with expression variation. Conclusions Expression variation among localities may reflect morphological differences in tumors that alter ratios of normal-to-tumor cells within biopsies. Phenotypic variation in tumors may arise from environmental variation or differences in host immune response that were undetectable in lip biopsies, potentially reflecting variation in host-tumor coevolutionary relationships among sites that differ in the time since DFTD arrival.

Natural herbivore populations have experienced uninterrupted pressures from direct and evident domestic-wildlife interactions and competition, to indirect or less obvious ones such as pathogen transmission. Thus, pathogen spillover between wild and domestic animals is a constant concern because the domestic-wildlife interface represents the ecological frontier in which pathogen transmission takes place in both directions. In Patagonian steppe communities, extensive sheep ranching and guanaco (Lama guanicoe) populations coexist, and guanaco have shown to be infected by pathogens such as Mycobacterium avium subspecies paratuberculosis (MAP) likely transmitted from livestock. MAP causes chronic enteritis and affects mostly domestic ruminants. We evaluated MAP prevalence and pathogen shedding in both species' faeces collected in non-shared and shared sites according to presence/absence of sheep and guanaco along a year, in four different seasons (autumn, winter, and spring 2018, and summer 2019). Our results indicate that MAP circulates in both sheep and guanaco populations with self-sustained transmission; however, both species differ in their levels of competence. We detected higher pathogen shedding in sites occupied by sheep, suggesting that sheep populations may be the main source of infection for susceptible animals due to their large numbers which drive MAP dynamics.

BackgroundSuicide results from complex interactions between biological, psychological, and socioeconomic factors. At the population level, the study of suicide rates and their environmental and social determinants allows us to disentangle some of these complexities and provides support for policy design and preventive actions.ObjectivesTo evaluate the associations between environmental and socioeconomic factors and demographically stratified suicide rates on large temporal and spatial scales.MethodThe dataset contains information about yearly suicides rates by sex and age from 2000 through 2017 along a 4,000 km latitudinal gradient. We used zero-inflated negative binomial models to evaluate the spatio-temporal influence of each environmental and socioeconomic variable on suicide rates at each sex/age combination.ResultsOverall, we found differential patterns of associations between suicide rates and explanatory variables by age and sex. Suicide rates in men increases in middle and high latitude regions and intermediate age classes. For adolescent and adult women, we found a similar pattern with an increase in suicide rates at middle and high latitudes. Sex differences measured by the male/female suicide rate ratio shows a marked increase with age. We found that cloudiness has a positive effect on suicide rates in both men and women 24 years old or younger. Regional poverty shows a major impact on men in age classes above 35 years old, an effect that was absent in women. Alcohol and marijuana consumption showed no significant effect sizes.ConclusionsOur findings support high spatio-temporal variability in suicide rates in interaction with extrinsic factors. Several strong differential impacts of environmental and socioeconomic variables on suicide rates depending on sex and age were detected. These results suggest that the design of public policies and interventions to mitigate the impact of the studied variables need to consider the local social and environmental contexts of target populations.

Individual hosts differ extensively in their competence for parasites, but traditional research has discounted this variation, partly because modeling such heterogeneity is difficult. This discounting has diminished as tools have improved and recognition has grown that some hosts, the extremely competent, can have exceptional impacts on disease dynamics. Most prominent among these hosts are the superspreaders, but other forms of extreme competence (EC) exist and others await discovery; each with potentially strong but distinct implications for disease emergence and spread. Here, we propose a framework for the study and discovery of EC, suitable for different host–parasite systems, which we hope enhances our understanding of how parasites circulate and evolve in host communities., Highlights A few members of host populations, so-called superspreaders, have disproportionate impacts on the risk of infectious disease emergence and spread. Several other forms of EC exist; some of which might be exceptionally protective. To discover and understand forms of EC, it is imperative to describe the distribution of, and covariation among, traits of individual hosts that mediate the many stages of host–parasite interactions. Here, we provide a framework to do so, emphasizing how interplay among host traits related to parasite exposure behavior, susceptibility, replicability of parasites on/in hosts, and transmissibility, comprise host competence. We hope this framework helps reveal new forms of EC and informs and improves management of disease risk.

The iconic Tasmanian devil (Sarcophilus harrisii) is endangered due to the transmissible cancer Devil Facial Tumour Disease (DFTD), of which there are two genetically independent subtypes (DFT1 and DFT2). While DFT1 and DFT2 can be differentially diagnosed using tumour biopsies, there is an urgent need to develop less-invasive biomarkers that can detect DFTD and distinguish between subtypes. Extracellular vesicles (EVs), the nano-sized membrane-enclosed vesicles present in most biofluids, represent a valuable resource for biomarker discovery. Here, we characterized the proteome of EVs from cultured DFTD cells using data-independent acquisition-mass spectrometry and an in-house spectral library of 1500 proteins. EVs from both DFT1 and DFT2 cell lines expressed higher levels of proteins associated with focal adhesion functions. Furthermore, hallmark proteins of epithelial-mesenchymal transition were enriched in DFT2 EVs relative to DFT1 EVs. These findings were validated in EVs derived from serum samples, revealing that the mesenchymal marker tenascin-C was also enriched in EVs derived from the serum of devils infected with DFT2 relative to those infected with DFT1 and healthy controls. This first EV-based investigation of DFTD increases our understanding of the cancers' EVs and their possible involvement in DFTD progression, such as metastasis. Finally, we demonstrated the potential of EVs to differentiate between DFT1 and DFT2, highlighting their potential use as less-invasive liquid biopsies for the Tasmanian devil.

1. The COVID-19 pandemic has highlighted the importance of efficient sampling strategies and statistical methods for monitoring infection prevalence, both in humans and reservoir hosts. Pooled testing can be an efficient tool for learning pathogen prevalence in a population. Typically pooled testing requires a second phase follow up procedure to identify infected individuals, but when the goal is solely to learn prevalence in a population, such as a reservoir host, there are more efficient methods for allocating the second phase samples. 2. To estimate pathogen prevalence in a population, this manuscript presents an approach for data integration with two-phased testing of pooled samples that allows more efficient estimation of prevalence with less samples than traditional methods. The first phase uses pooled samples to estimate the population prevalence and inform efficient strategies for the second phase. To combine information from both phases, we introduce a Bayesian data integration procedure that combines pooled samples with individual samples for joint inferences about the population prevalence. 3. Data integration procedures result in more efficient estimation of prevalence than traditional procedures that only use individual samples or a single phase of pooled sampling. 4. The manuscript presents guidance on implementing the first phase and second phase sampling plans using data integration. Such methods can be used to assess the risk of pathogen spillover from reservoir hosts to humans, or to track pathogens such as SARS-CoV-2 in populations.

Background Transmissible cancers lie at the intersection of oncology and infectious disease, two traditionally divergent fields for which gene expression studies are particularly useful for identifying the molecular basis of phenotypic variation. In oncology, transcriptomics studies, which characterize the expression of thousands of genes, have identified processes leading to heterogeneity in cancer phenotypes and individual prognoses. More generally, transcriptomics studies of infectious diseases characterize interactions between host, pathogen, and environment to better predict population-level outcomes. Tasmanian devils have been impacted dramatically by a transmissible cancer (devil facial tumor disease; DFTD) that has led to widespread population declines. Despite initial predictions of extinction, populations have persisted at low levels, due in part to heterogeneity in host responses, particularly between sexes. However, the processes underlying this variation remain unknown. Results We sequenced transcriptomes from healthy and DFTD-infected devils, as well as DFTD tumors, to characterize host responses to DFTD infection, identify differing host-tumor molecular interactions between sexes, and investigate the extent to which tumor gene expression varies among host populations. We found minimal variation in gene expression of devil lip tissues, either with respect to DFTD infection status or sex. However, 4,088 genes were differentially expressed in tumors among our sampling localities. Pathways that were up- or downregulated in DFTD tumors relative to normal tissues exhibited the same patterns of expression with greater intensity in tumors from localities that experienced DFTD for longer. No RNA sequence variants were associated with expression variation. Conclusions Expression variation among localities may underly phenotypic variation in the tumor, potentially manifesting in morphological differences that alter ratios of normal-to-tumor cells within biopsies. Phenotypic variation in tumors may arise from environmental variation or differences in host immune response that were undetectable in lip biopsies, potentially reflecting variation in host-tumor coevolutionary relationships among sites that differ in the time since DFTD arrival.

SARS-CoV-2 spreads quickly in dense populations, with serious implications for universities, workplaces, and other settings where exposure reduction practices are difficult to implement. Rapid screening has been proposed as a tool to slow the spread of the virus; however, many commonly used diagnostic tests (e.g., RT-qPCR) are expensive, difficult to deploy (e.g., require a nasopharyngeal specimen), and have extended turn-around times. We evaluated testing regimes that combined diagnostic testing using qPCR with high-frequency screening using a novel reverse-transcription loop-mediated isothermal amplification (RT-LAMP, herein LAMP) assay. We used a compartmental susceptible-exposed-infectious-recovered (SEIR) model to simulate screening of a university population. We also developed a Shiny application to allow administrators and public health professionals to develop optimal testing strategies given site-specific assumptions about testing investment, target population, and cost. The frequency of screening, especially when pooling samples, was more important for minimizing epidemic size than test sensitivity, behavioral compliance, contact tracing capacity, and time between testing and results. Our results suggest that when testing budgets are limited, it is safer and more cost-effective to allocate the majority of funds to screening. Rapid, cost-effective, and scalable screening tests, like LAMP, should be viewed as critical components of SARS-CoV-2 testing in high-density populations.

Infectious diseases are strong drivers of wildlife population dynamics, however, empirical analyses from the early stages of pathogen emergence are rare. Tasmanian devil facial tumour disease (DFTD), discovered in 1996, provides the opportunity to study an epizootic from its inception. We use a pattern-oriented diffusion simulation to model the spatial spread of DFTD across the species' range and quantify population effects by jointly modelling multiple streams of data spanning 35 years. We estimate the wild devil population peaked at 53 000 in 1996, less than half of previous estimates. DFTD spread rapidly through high-density areas, with spread velocity slowing in areas of low host densities. By 2020, DFTD occupied >90% of the species' range, causing 82% declines in local densities and reducing the total population to 16 900. Encouragingly, our model forecasts the population decline should level-off within the next decade, supporting conservation management focused on facilitating evolution of resistance and tolerance.

Emergence to endemism The emergence of a devastating transmissible facial cancer among Tasmanian devils over the past few decades has caused substantial concern for their future because these animals are already threatened by a regional distribution and other stressors. Little is known about the overall history and trajectory of this disease. Patton et al. used an epidemiological phylodynamic approach to reveal the pattern of disease emergence and spread. They found that low Tasmanian devil densities appear to be contributing to slower disease growth and spread, which is good news for Tasmanian devil persistence and suggests that care should be taken when considering options for increasing devil populations. Science , this issue p. eabb9772

Devil facial tumor disease (DFTD) is a transmissible cancer affecting Tasmanian devils Sarcophilus harrisii. The disease has caused severe population declines and is associated with demographic and behavioral changes, including earlier breeding, younger age structures, and reduced dispersal and social interactions. Devils are generally solitary, but social encounters are commonplace when feeding upon large carcasses. DFTD tumors can disfigure the jaw and mouth and so diseased individuals might alter their diets to enable ingestion of alternative foods, to avoid conspecific interactions, or to reduce competition. Using stable isotope analysis (δ13C and δ15N) of whiskers, we tested whether DFTD progression, measured as tumor volume, affected the isotope ratios and isotopic niches of 94 infected Tasmanian devils from six sites in Tasmania, comprising four eucalypt plantations, an area of smallholdings and a national park. Then, using tissue from 10 devils sampled before and after detection of tumors and 8 devils where no tumors were detected, we examined whether mean and standard deviation of δ13C and δ15N of the same individuals changed between healthy and diseased states. δ13C and δ15N values were generally not related to tumor volume in infected devils, though at one site, Freycinet National Park, δ15N values increased significantly as tumor volume increased. Infection with DFTD was not associated with significant changes in the mean or standard deviation of δ13C and δ15N values in individual devils sampled before and after detection of tumors. Our analysis suggests that devils tend to maintain their isotopic niche in the face of DFTD infection and progression, except where ecological conditions facilitate a shift in diets and feeding behaviors, demonstrating that ecological context, alongside disease severity, can modulate the behavioral responses of Tasmanian devils to DFTD., Tasmanian devils generally maintain their isotopic niche in the face of infection and progression of devil facial tumor disease. The exception was where ecological conditions facilitated a shift in diets and feeding behaviors, such as at Freycinet National Park. Ecological context, alongside disease severity, can modulate the behavioral responses of Tasmanian devils to DFTD. ​

The impact of emerging infectious diseases is increasingly recognised as a major threat to wildlife. Wild populations of the endangered Tasmanian devil, Sarcophilus harrisii, are experiencing devastating losses from a novel transmissible cancer, devil facial tumour disease (DFTD), however, despite the rapid decline of this species, there is currently no information on the presence of haemoprotozoan parasites. In the present study, 95 Tasmanian devil blood samples were collected from four populations in Tasmania, Australia, which underwent molecular screening to detect four major groups of haemoprotozoa: (i) trypanosomes, (ii) piroplasms, (iii) Hepatozoon, and (iv) haemosporidia. Sequence results revealed Trypanosoma infections in 32/95 individuals. Trypanosoma copemani was identified in 10 Tasmanian devils from three sites and a second Trypanosoma sp. was identified in 22 individuals that were grouped within the poorly described T. cyclops clade. A single blood sample was positive for Babesia sp., which most closely matched Babesia lohae. No other blood protozoan parasite DNA was detected. This study provides the first insight into haemoprotozoa from the Tasmanian devil and the first identification of Trypanosoma and Babesia in this carnivorous marsupial.

Spontaneous tumor regression has been documented in a small proportion of human cancer patients, but the specific mechanisms underlying tumor regression without treatment are not well understood. Tasmanian devils are threatened with extinction from a transmissible cancer due to universal susceptibility and a near 100% case fatality rate. In over 10,000 cases

For ectothermic species with broad geographical distributions, latitudinal/altitudinal variation in environmental temperatures (averages and extremes) is expected to shape the evolution of physiological tolerances and the acclimation capacity (i.e., degree of phenotypic plasticity) of natural populations. This can create geographical gradients of selection in which environments with greater thermal variability (e.g., seasonality) tend to favor individuals that maximize performance across a broader range of temperatures compared to more stable environments. Although thermal acclimation capacity plays a fundamental role in this context, it is unknown whether natural selection targets this trait in natural populations. Additionally, understanding whether and how selection acts on thermal physiological plasticity is also highly relevant to climate change and biological conservation. Here, we addressed such an important gap in our knowledge in the northernmost population of the four‐eyed frog, Pleurodema thaul. We measured plastic responses of critical thermal limits for activity, behavioral thermal preference, and thermal sensitivity of metabolism to acclimation at 10 and 20°C. We monitored survival during three separate recapture efforts and used mark‐recapture integrated into an information‐theoretic approach to evaluate the relationship between survivals as a function of the plasticity of thermal traits. Overall, we found no evidence that thermal acclimation in this population is being targeted by directional selection, although there might be signals of selection on individual traits. According to the most supported models, survival increased in individuals with higher tolerance to cold when cold‐acclimated, probably because daily low extremes are frequent during the cooler periods of the year. Furthermore, survival increased with body size. However, in both cases, the directional selection estimates were nonsignificant, and the constraints of our experimental design prevented us from evaluating more complex models (i.e., nonlinear selection).

Understanding the genetic basis of disease-related phenotypes, such as cancer susceptibility, is crucial for the advancement of personalized medicine. Although most cancers are somatic in origin, a small number of transmissible cancers have been documented. Two such cancers have emerged in the Tasmanian devil (Sarcophilus harrisii) and now threaten the species with extinction. Recently, cases of natural tumor regression in Tasmanian devils infected with the clonally contagious cancer have been detected. We used whole-genome sequencing and FST-based approaches to identify the genetic basis of tumor regression by comparing the genomes of seven individuals that underwent tumor regression with those of three infected individuals that did not. We found three highly differentiated candidate genomic regions containing several genes related to immune response and/or cancer risk, indicating that the genomic basis of tumor regression was polygenic. Within these genomic regions, we identified putative regulatory variation in candidate genes but no nonsynonymous variation, suggesting that natural tumor regression may be driven, at least in part, by differential host expression of key loci. Comparative oncology can provide insight into the genetic basis of cancer risk, tumor development, and the pathogenicity of cancer, particularly due to our limited ability to monitor natural, untreated tumor progression in human patients. Our results support the hypothesis that host immune response is necessary for triggering tumor regression, providing candidate genes that may translate to novel treatments in human and nonhuman cancers.

Reconstructing species’ demographic histories is a central focus of molecular ecology and evolution. Recently, an expanding suite of methods leveraging either the sequentially Markovian coalescent (SMC) or the site-frequency spectrum has been developed to reconstruct population size histories from genomic sequence data. However, few studies have investigated the robustness of these methods to genome assemblies of varying quality. In this study, we first present an improved genome assembly for the Tasmanian devil using the Chicago library method. Compared with the original reference genome, our new assembly reduces the number of scaffolds (from 35,975 to 10,010) and increases the scaffold N90 (from 0.101 to 2.164 Mb). Second, we assess the performance of four contemporary genomic methods for inferring population size history (PSMC, MSMC, SMC++, Stairway Plot), using the two devil genome assemblies as well as simulated, artificially fragmented genomes that approximate the hypothesized demographic history of Tasmanian devils. We demonstrate that each method is robust to assembly quality, producing similar estimates of Ne when simulated genomes were fragmented into up to 5,000 scaffolds. Overall, methods reliant on the SMC are most reliable between ∼300 generations before present (gbp) and 100 kgbp, whereas methods exclusively reliant on the site-frequency spectrum are most reliable between the present and 30 gbp. Our results suggest that when used in concert, genomic methods for reconstructing species’ effective population size histories 1) can be applied to nonmodel organisms without highly contiguous reference genomes, and 2) are capable of detecting independently documented effects of historical geological events.

Australia’s 81 bat species play vital ecological and economic roles via suppression of insect pests and maintenance of native forests through pollination and seed dispersal. Bats also host a wide diversity of coronaviruses globally, including several viral species that are closely related to SARS-CoV-2 and other emergent human respiratory coronaviruses. Although there are hundreds of studies of bat coronaviruses globally, there are only three studies of bat coronaviruses in Australian bat species, and no systematic studies of drivers of shedding. These limited studies have identified two betacoronaviruses and seven alphacoronaviruses, but less than half of Australian species are included in these studies and further research is therefore needed. There is no current evidence of spillover of coronaviruses from bats to humans in Australia, either directly or indirectly via intermediate hosts. The limited available data are inadequate to determine whether this lack of evidence indicates that spillover does not occur or occurs but is undetected. Conversely, multiple international agencies have flagged the potential transmission of human coronaviruses (including SARS CoV-2) from humans to bats, and the consequent threat to bat conservation and human health. Australia has a long history of bat research across a broad range of ecological and associated disciplines, as well as expertise in viral spillover from bats. This strong foundation is an ideal platform for developing integrative approaches to understanding bat health and sustainable protection of human health.

Knowledge of the ecological dynamics between hosts and pathogens during the initial stages of disease emergence is crucial to understanding the potential for evolution of new interspecific interactions. Tasmanian devil ( Sarcophilus harrisii ) populations have declined precipitously owing to infection by a transmissible cancer (devil facial tumour disease, DFTD) that emerged approximately 20 years ago. Since the emergence of DFTD, and as the disease spreads across Tasmania, the number of devils has dropped up to 90% across 80% of the species's distributional range. As a result, the disease is expected to act as a strong selective force on hosts to develop mechanisms of tolerance and/or resistance to the infection. We assessed the ability of infected devils to cope with infection, which translates into host tolerance to the cancer, by using the reaction norm of the individual body condition by tumour burden. We found that body condition of infected hosts is negatively affected by cancer progression. Males and females presented significant differences in their tolerance levels to infection, with males suffering declines of up to 25% of their body condition, in contrast to less than 5% in females. Sex-related differences in tolerance to cancer progression may select for changes in life-history strategies of the host and could also alter the selective environment for the tumours.

When dispersal is not an option to evade warming temperatures, compensation through behavior, plasticity, or evolutionary adaptation is essential to prevent extinction. In this work, we evaluated whether there is physiological plasticity in the thermal performance curve (TPC) of maximum jumping speed in individuals acclimated to current and projected temperatures and whether there is an opportunity for behavioral thermoregulation in the desert landscape where inhabits the northernmost population of the endemic frog Pleurodema thaul. Our results indicate that individuals acclimated to 20°C and 25°C increased the breath of their TPCs by shifting their upper limits with respect to when they were acclimated at 10°C. In addition, even when dispersal is not possible for this population, the landscape is heterogeneous enough to offer opportunities for behavioral thermoregulation. In particular, under current climatic conditions, behavioral thermoregulation is not compulsory as available operative temperatures are encompassed within the population TPC limits. However, for severe projected temperatures under climate change, behavioral thermoregulation will be required in the sunny patches. In overall, our results suggest that this population of Pleurodema thaul will be able to endure the worst projected scenario of climate warming as it has not only the physiological capacities but also the environmental opportunities to regulate its body temperature behaviorally.