Evolution, Medicine, and Public Health

The 17th Ebola outbreak in the Democratic Republic of the Congo, announced on 15 May 2026, was attributed to Bundibugyo ebolavirus (BDBV). Although case isolation is the main control strategy, its effectiveness is compromised when patients escape isolation facilities before recovery. Between 14 May and 17 June 2026, 175 individuals reportedly left isolation facilities without formal discharge across Ituri Province. We assessed how this "isolation leakage" affects community transmission. We refined the SEIHFR framework to distinguish undetected community infections, detected but not-yet-isolated cases, isolated individuals, leakage, funeral-associated transmission, and removals. Using Bayesian inference, we fitted the model to daily Ituri surveillance data, escapee counts, and isolation census records. We estimated the leakage rate, reporting and detection probabilities, and the transmission rate, while fixing other parameters based on the BDBV literature. The model reproduced confirmed cases, deaths, discharges, and escapees. We estimated R_0=3.67 (95% HDI: 2.0-5.7), a leakage rate of {rho} {approx} 0.034 day^-1 (0.022-0.051), and high contact-tracing-driven detection (p_d {approx} 0.91-0.99). Leakage increased the detection-dependent reproduction number [R](p_d) from approximately 3.2 to above 5. Eliminating leakage reduced cumulative infections by about one-third, from 1,120 to 764, while the minimum detection level required for control increased from p_d [≥] 0.73 without leakage to p_d [≥] 0.87 at the fitted leakage rate. Shortening time to isolation prevented the most infections (73.4%; 59-84), followed by reducing leakage (29.7%; 14-52) and re-isolating escapees (12.6%; 6-24). Delaying leakage reduction until week 4 reduced its benefit from about 27% to below 2%. Isolation leakage represents a major transmission pathway that has until now gone largely unmeasured. While rapid initiation of isolation is highly beneficial, it cannot compensate for permeable isolation; therefore, early, community-driven efforts to control leakage, embedded within a multilayered response, are critical.

Across different modalities, signals play a core role in attracting mates and influencing mating success. In several non-human primate species, females produce calls during mating that are thought to promote male competition over receptive females. The extent to which social system characteristics modulate the function of copulation calls remains less clear. We studied copulation calls in wild Guinea baboons (Papio papio), who live in a multilevel society structured around units in which females associate and mate almost exclusively with a single male. We hypothesised that females use copulation calls as an indirect form of mate competition, with competition increasing in larger units. In addition, we hypothesised that females are more likely to mate again after calling. We analysed 6116 copulations between 2014 and 2025, involving 99 reproductively active females and 78 subadult and adult males. Females produced copulation calls in 72.7% of copulations, with large inter-individual variation. Neither unit size nor its interaction with the female's swelling size or the presence of simultaneously receptive females affected the probability of calling. A survival analysis with a subset of the data (2353 copulations) revealed no effect of calling on the latency to the next mating. Our results render the hypothesis that female Guinea baboons use calls in indirect mate competition unlikely. Yet, the probability of calling varied with sexual swelling size, suggesting that calls signal female fertility. Possibly, Guinea baboon copulation calls represent an evolutionary remnant, no longer under selective pressure, and can be considered index signals of female fertility.

Rapid evolution allows populations to persist in environments where they would otherwise go extinct. This phenomenon, known as evolutionary rescue, is typically studied in the framework of biological evolution, yet adaptive traits can also arise and spread through cultural evolution. The present study developed a stochastic eco-evolutionary model to compare rescue probabilities through biological and cultural evolution. Transmission bias governed the rescue probability under cultural evolution by setting how readily a rare adaptive trait was copied. Conformity bias suppressed population persistence because a rare trait was the least likely to be copied. Content bias toward the adaptive trait enabled evolutionary rescue when social learning was rapid, but it typically yielded a lower rescue probability than biological evolution. Only anticonformity bias, together with a high social learning rate, exceeded the rescue probability of biological evolution by enabling the adaptive trait to be established more rapidly. These results demonstrate that transmission bias alters the demographic consequences of cultural evolution and highlight the importance of transmission processes in evolutionary rescue theory. Understanding how adaptive behaviours are socially transmitted may also improve predictions of animal population persistence and inform conservation efforts in rapidly changing environments.

The increasing incidence of H5N1 influenza virus transmission from animal species to humans has heightened concerns about an imminent H5N1 pandemic. Prior studies using recombinant hemagglutinin and neuraminidase proteins have reported age-dependent cross-reactivity to H5N1, attributed to immune imprinting from an individual's first influenza virus exposure. However, whether this pattern holds when using whole inactivated virus (WIV), capturing antibodies against diverse viral proteins, and is stable over time remains unknown. We therefore aimed to determine whether H5N1 cross-reactivity of pre-existing antibodies to whole virus follows an age-dependent or imprinting-specific pattern, and whether this pattern is stable over a five-year period. To this end, we measured serum antibody levels in adolescents, adults and seniors by ELISA using whole inactivated H5N1 virus as antigen rather than purified proteins. Detectable, albeit generally low, levels of H5N1-reactive antibodies were present in most individuals, irrespective of age. Comparison of antibody levels against H5N1 with those to five historical influenza virus strains revealed a consistent positive correlation between H5N1-reactive antibodies and responses to the H1N1pdm09 strain A/California/7/2009 (CA), across all age groups. Using unbiased clustering of antibody titers against H5N1, CA, and the H3N2 strain A/Perth/16/2009 (PE), we identified seven distinct age-transcending antibody profiles. These profiles covered individuals with varying titers to all three included viruses but also identified individuals with high anti-CA levels, yet low anti-H5N1 levels and vice versa. Moreover, despite stable antibody levels over a five-year interval in the study population, individual antibody levels and profiles fluctuated considerably over this period. Taken together, our results confirm the presence of H5N1-reactive antibodies in human sera and their association with previously circulating strains. However, they also caution against inferring antibody levels against a new strain based solely on responses to antigenically related strains and highlight the limitations of extrapolating immune status from single timepoint measurements.

Dissecting the complexity of antibody responses in orthopoxvirus (OPXV) infected individuals is essential for elucidating protective mechanisms and identifying candidate protective immunogens. Here, we profiled the acute humoral response in 51 mpox cases, showing distinct IgG trajectories among multiple antigens alongside the rise of plasma neutralizing activities to plateau within 6 weeks after symptom onset. Utilizing a single-cell transcriptomic and BCR sequencing based antigen-agnostic mAb isolation workflow, we further generated monoclonal antibodies (mAbs) from 254 expanded peripheral B cell clones of 3 patients. We discerned 97 specific mAbs recognizing at least 12 different OPXV proteins via integrated screening approaches, which comprised neutralizing antibodies binding unconventional viral targets and antibodies exhibiting extraordinary in vitro and in vivo anti-OPXV effects. The number of OPXV-specific mAbs recovered per donor reflected the percentage of expanded clones among circulating B cells. More interestingly, we demonstrated that the inferred unmutated common ancestors (UCAs) of neutralizing antibody clones did not necessarily react with OPXV, implying that OPXV neutralizing antibodies might frequently originate from B cells previously activated by unknown antigens. Our work establishes an efficient workflow for antigen-agnostic isolation of pathogen specific mAbs and reveals previously unclarified features of antibody responses induced by acute MPXV infection.

Importance: Chronic stress may contribute to adverse health outcomes through cumulative physiologic dysregulation. Allostatic load (AL), a composite measure of multisystem physiologic burden, may capture biologic effects of structural, social, and psychosocial stress not reflected by self-reported measures. Objective: To evaluate racial and ethnic differences in AL among women with familial cancer risk and examine how socioeconomic status, psychosocial factors, clinical characteristics, and health behaviors contribute to variations in AL. Design: Cross-sectional study of underrepresented minority participants enrolled in the HERSTORY cohort from October 2023 through September 2025, with comparison participants from the UCLA ATLAS biobank. Setting: UCLA academic health system. Participants: The study included 303 racially and ethnically diverse female HERSTORY participants aged [≥]35 years with a family history of cancer and matched non-Hispanic White female ATLAS participants (n=709). Exposures: Race and ethnicity, age, neighborhood deprivation, cancer history and stage, depression, perceived stress, cancer worry, and physical activity. Main Outcomes and Measures: The primary outcome was AL, calculated from cardiometabolic and organ-function measures. A secondary index incorporated race- and ethnicity-specific neutrophil-to-lymphocyte ratio (NLR) derived from 326,826 women in the UCLA Health population. Multivariable regression models evaluated factors associated with elevated AL. Results: Compared with matched non-Hispanic White participants, Black and Asian/Pacific Islander HERSTORY participants had significantly higher AL after adjustment. Hispanic/Latina participants did not have significantly elevated AL. Older age, greater area-level socioeconomic deprivation, and depression were independently associated with higher AL. Prior cancer diagnosis, cancer worry and perceived stress were not significantly associated with AL, whereas regular physical activity was associated with lower AL. Among cancer patients, advanced stage was associated with greater AL. Conclusions and Relevance: This study demonstrates elevated AL among understudied racial/ethnic minority groups with familial cancer risk and identifies associations with neighborhood deprivation, depression, and physical activity. The association between cancer stage and AL suggests that physiologic stress may reflect variation in cancer burden. The lack of association with perceived stress and cancer worry further indicates that physiologic and self-reported psychosocial measures capture distinct dimensions of stress. The development of race/ethnicity-specific NLR thresholds derived from large population samples provide a benchmark for future studies.

Genomic instability is a major driver of tumor evolution, promoting diversification and adaptation while simultaneously increasing the accumulation of deleterious alterations. How tumor populations balance these opposing effects remains poorly understood. Here, we introduce a computational framework that explicitly represents diploid genomes, functional gene classes, point mutations, and chromosome-segregation errors in spatially constrained and well-mixed tumor populations. We identify a viability boundary separating sustained tumor expansion from instability-induced population collapse. Within the viable regime, mutation and selection generate a stable distribution of genomic-instability classes that is accurately captured by an analytical replicator--mutator description. Near the viability boundary, tumor dynamics exhibit prolonged extinction transients and strong sensitivity to stochastic fluctuations, with important differences between solid and liquid architectures. Chromosomal alterations further modify growth by creating transient benefits through increased gene dosage and genetic redundancy, while ultimately increasing genomic fragility. Finally, simulated interventions show that eliminating low-instability subpopulations or increasing the global mutational burden can displace tumors beyond their viability boundary and trigger irreversible collapse. These results identify genome instability as both an evolutionary advantage and an intrinsic vulnerability, providing a quantitative framework for developing therapies that exploit the limits of tumor evolution.

Infections with bacteria which have evolved multi-drug resistance (MDR) cause millions of deaths worldwide. Large-scale efforts are gathering genotypic and phenotypic data on MDR bacteria, but methods for learning the structure, diversity, and predictors of evolutionary pathways to MDR have yet to take full advantage of these data. Here, we use evolutionary accumulation modelling (EvAM), an emerging class of machine learning methods with roots in cancer progression, to infer these evolutionary pathways across ESKAPEE pathogens (seven bacterial species that dominate health burdens), using a database of over 635k genotyped phenotypic observations from around the world. We identify global patterns in MDR evolutionary pathways, remarkably shared across multiple ESKAPEE species. Species-specific deviations from these stereotypical pathways are connected with geographical and demographic covariates, facilitating predictions of future MDR evolution. We verify these predictions with several hundred new phenotypes from ESKAPEE samples spanning decades of clinical infections in sub-Saharan Africa, demonstrating the capacity to forecast future MDR evolution from these inferred shared pathways.

Vaccine effectiveness (VE) estimates can vary widely between years and populations, even for the same vaccine. Estimated VE is known to be sensitive to susceptible depletion and differences in pre-vaccination infection risk between vaccinated and unvaccinated populations. However, how variation in pre-vaccination risk within and between the two groups affects VE estimates over time remains unclear. This uncertainty is especially important given negative VE estimates. We investigated the difference between estimated VE and true vaccine protection considering continuous distributions of pre-vaccination infection risk under three scenarios. When the vaccinated and unvaccinated populations differ in their mean risk, estimated VE can be higher or lower than true vaccine protection. Similar patterns arise when both populations share identical means but different risk distributions. Finally, if infection-derived immunity lasts longer than vaccine protection, annual VE estimates can vary by tens of percentage points between years despite constant true vaccine protection. These theoretical results underscore that VE studies estimate contrasting risk between vaccinated and unvaccinated individuals in a particular time and place, and VE estimates can vary counterintuitively between years and populations even with constant vaccine-induced protection. Explaining variability in estimated VE thus requires a more complete understanding of populations' distributions of infection risk.

Purpose Despite the high documented prevalence of hunger and poor mental health in adolescent girls and young women (AGYW) in South Africa, this relationship remains understudied, with existing studies limited by their cross-sectional designs. This longitudinal study aimed to identify the association of hunger trajectories with anxiety and depressive symptoms, and hope in AGYW. Methods We used secondary data from the HIV Prevention Trials Network (HPTN) -068 conducted in rural Agincourt, South Africa. Complete data from 1779 AGYW collected at baseline (2011/12) and three annual follow-up visits were used. Hunger trajectories, measured using the Household Hunger Scale, were estimated via Group-Based Trajectory Modelling. Self-reported incident anxiety and depressive symptoms and hope were assessed based on AGYWs last two follow-up visits. Covariate adjusted modified Poisson regression models estimated the association between hunger trajectories and incident anxiety symptoms, incident depressive symptoms, and hope. Results Moderate-severe hunger was prevalent in 11.0%, 10.8%, and 6.0% of the households at baseline, follow-up 1, and 2, respectively. Incident anxiety symptoms were reported by 4.5%, incident depressive symptoms by 20.0% and hopelessness by 52.8% of the AGYW. Two hunger trajectories were identified- no hunger (82%) and marginal hunger (18%). Hunger trajectories were not associated with incident anxiety symptoms [RR:1.09, 95% CI: 0.55, 2.18], incident depressive symptoms [RR: 0.97; 95% CI: 0.72, 1.33] nor hope [RR: 1.00; 95% CI: 0.81, 1.23] in AGYW. Conclusion Better understanding of the factors that promote resiliency and mental health of AGYW in this setting is warranted to inform the design of interventions.

Background National childhood respiratory pathogen spectra are diversifying nearly everywhere - within-country diversity rose in 203 of 204 countries between 1990 and 2023 - yet whether countries are diversifying toward a common spectrum or along divergent paths is unknown. We quantified between-country compositional distance of national pathogen spectra over the same period. Methods We built national pathogen share vectors from Global Burden of Disease Study 2023 lower respiratory infection etiologic attributions (26 pathogens, 204 countries, ages 0-19 years) at five timepoints spanning 1990-2023. Between-country distance was measured as all pairwise Jensen-Shannon divergences (JSD; primary) and Bray-Curtis dissimilarities, with Baselga and Jaccard decompositions; robustness was assessed across metrics, pathogen panels, low-count thresholds and a balanced panel of 107 countries. Results Mean pairwise JSD rose from 0.0084 in 1990 to 0.0283 in 2023 (+238%; trend p = 0.030), peaking in 2021 (+283%) with a partial 2023 pullback. Bray-Curtis dissimilarity rose +120% and the balanced panel +423%. Divergence was entirely balanced variation (share reallocation), with spectrum richness rising from 18.5 to 21.1 of 26 pathogens. Dispersion rose fastest for influenza (coefficient of variation 0.03 to 0.55) and respiratory syncytial virus (0.08 to 0.48). Within-region distance rose in every computable GBD super-region (five of seven): divergence occurs within regions, not between blocs. Conclusions National spectra are re-sorting along country-specific axes as vaccine-preventable dominance recedes at different speeds. Diversification is universal, but convergence is absent: the transition at the etiologic-spectrum level is asynchronous and path-dependent, with implications for empirical treatment policy and pathogen surveillance.

Sicyoidochytrium minutum DNA virus (SmDNAV) was isolated several years ago from a protist host of family Thraustochytriaceae of the class Labyrinthulomycetes. This virus shared little similarity to other viruses in gene content and protein sequences, albeit seemingly belonging to the phylum Nucleocytoviricota. By extensive searches in genomic and metagenomic sequence databases, we identified numerous long contigs related to the SmDNAV genome and analyzed proteins shared by these putative viruses. Phylogenetic analyses place these viruses within the class Megaviricetes, outside of all established orders, and as a sister group to the clade combining families Mamonoviridae and Manesviridae. Homologs of SmDNAV proteins were found in association (either integrated or co-sequenced) with other Labyrinthulomycetes and Rhodophyta protists from diverse marine and freshwater environments. Consequently, we propose SmDNAV as the prototype member of a new order, provisionally named Ariadnavirales, within class Megaviricetes, phylum Nucleocytoviricota. Members of Ariadnavirales have lost most of the genes encoding components of the replication and transcription systems that are otherwise conserved in nucleocytoviricots, suggestive of transition to genome replication and expression dependent on the host nucleus.

The shape of density-dependence governs species persistence, and ecosystem stability. Yet, whether per-capita growth declines sublinearily, or superlinearily with density remains hotly debated. Growth rates across the tree of life have been shown to decline sublinearly with density, whereas theory founded on resource competition predicts the opposite. Here, we resolve this discrepancy and show that sublinearity can readily emerge from geometric constraints on consumer interactions. By linking inter individual spacing, movement and interference rates, we derive two limiting-interference regimes, one of which the well-mixed limit recovers the form of classic Beddington DeAngelis interference response. We then developed an individual-based model from first principles which reproduces the derived sublinearity response, and further use empirical data from published consumer-resource experiments that also bears the signature of sublinear density-dependence. Further, embedding the interference mechanisms underlying the emergence of sublinear density-dependence in coexistence theory opens a new regime for species coexistence where classical theory fails to predict. Our framework indicates that non-consumptive interactions are not merely a correction to resource competition but might be a distinct axis along which diverse communities may potentially coexist.

Bulk telomere length measured from tumour sequencing is routinely interpreted as a property of the cancer cells. However, a tumour specimen is a mixture, and the patient who supplies it has a telomere length of their own. Here I re-analyse published pan-cancer telomere estimates and ask how much of a tumour's telomere length is patient-specific. A calibration step comes first. Whole-genome and low-pass estimates recover the known cross-sectional attrition of leukocyte telomeres with age, at 26.6 bp per year in blood normals, whereas whole-exome estimates do not. After adjustment for cancer type, sequencing centre and sex, the exome slope is minus 0.6 bp per year. In 684 blood-normal aliquots sequenced by both assays, the whole-genome estimate declines at 38.9 bp per year, whereas the exome estimate from the same DNA shows no detectable decline. The difference between assays is 41.5 bp per year, with P = 3 x 10^-10. Because exome data constitute 78.6% of the original resource, downstream analyses use only whole-genome and low-pass libraries. Within those data, tumour telomere length tracks the patient's matched-normal telomere length. The Spearman correlation is 0.395 in TCGA, with positive associations in 22 of 23 cancer types. This finding replicates in PCAWG using a different telomere estimator, with a correlation of 0.472 and positive associations in all 24 histologies examined. Adjustment for cancer type, sequencing centre and library type leaves a regression coefficient of 0.385. The association is also stable after adjustment for age, sex, tumour purity, leukocyte fraction, ploidy, sequencing coverage and continental ancestry, with coefficients ranging from 0.406 to 0.429. Pure normal-cell admixture is rejected as the sole explanation. Under a two-compartment mixture model, the coefficient for host telomere length is expected to equal 1 and the host-by-purity interaction to equal minus 1. These restrictions are jointly rejected with P = 0.001. Tumour purity, leukocyte fraction and age each explain only about 1 to 3% of within-cohort variance and do not alter the cross-cancer ranking. By contrast, the between-cohort coefficient is not directly interpretable. Its apparent near one-to-one relationship with tissue-associated telomere length depends strongly on which tissue supplies the matched-normal reference and on the statistical spread of that predictor, falling to 0.44 when organ-matched solid tissue is used. Bulk tumour telomere length is therefore a composite phenotype containing a replicated patient-specific component. Telomere biomarker studies should include matched-normal telomere length as a covariate rather than treating tumour telomere length as exclusively tumour-intrinsic.

Circadian clocks enable mosquitoes to anticipate recurring environmental variations and coordinate behaviors critical for survival and disease transmission, such as locomotion, reproduction, host-seeking, and blood-feeding, with times of day when performance is maximal. In Aedes aegypti, locomotor activity follows a robust diurnal rhythm shaped by endogenous circadian clocks and environmental cues, among which light has been shown to be the primary source of temporal information. While early studies established the role of light in regulating locomotor activity, behavior, oviposition and pupation, it remains unclear which features of a light cycle drive changes in circadian rhythms. This question is increasingly relevant as Ae. aegypti is frequently exposed to artificial and dynamic lighting conditions in urban environments. Here, we investigated how transient changes in light schedules influence circadian rhythms in locomotor activity by systematically manipulating the timing, duration, and direction of light exposure. Using a high-throughput assay, we tested over 1900 individuals, including wild-type and timeless knockout mutants, and showed that a single day of al tered lighting is sufficient to induce robust phase shifts, with no evidence of masking effects. A 6-hour light pulse was sufficient to re-entrain mosquitoes regardless of the timing of the pulse, and phase shifts were primarily driven by the offset time of the light pulse, indicating that light-offset acts as a major zeitgeber. Together, these findings challenge conventional assumptions about the timescale of circadian synchronization and highlight the remarkable plasticity of mosquito behavior in response to anthropogenic light. Eventually, these effects could explain the rapid adaptation of the species to urban environments and have potential consequences for disease transmission dynamics.

Background: The biological mechanism linking rainfall with leptospirosis transmission is well established, but rigorous quantitative evidence for the insular Caribbean remains scarce, limited mostly to descriptive reports of post-hurricane outbreaks. We aimed to quantify the association between rainfall and leptospirosis incidence in the Dominican Republic, where leptospirosis is endemic, between 2012 and 2026 using a distributed-lag approach. Methods: We conducted an ecological time-series study complemented by a province panel with fixed effects. Case data (5,412 valid cases) were obtained from the national surveillance system (SIP-0276FA51); rainfall data were obtained from 15 INDOMET rain gauge stations across 13 provinces (2000 to 2026). We calculated the cross-correlation function between lagged monthly rainfall (0 to 6 months) and case counts, fitted a negative binomial distributed-lag regression model (lags 0 to 3 months) adjusted for seasonality and trend, triangulated findings with a 13-province fixed-effects panel, compared four rainfall exposure metrics, assessed extreme-rainfall threshold sensitivity, and estimated the population attributable fraction (PAF) with a parametric bootstrap. Results: The rainfall-case association peaked at a 1-month lag (r = 0.551; 95 % CI 0.437-0.647; p < 0.001) and remained significant through 3 months. In the distributed-lag model, all four lags were independently significant, with the 1-month lag showing the strongest effect (incidence rate ratio [IRR] = 1.156 per additional 50mm; 95 % CI 1.090-1.226; p < 0.001). The province panel yielded an almost identical 1-month lag effect (IRR = 1.147; 95 % CI 1.127-1.167). Rainfall above the historical 90th percentile increased case risk the following month (rate ratio = 1.95), with effect magnitude increasing monotonically with threshold stringency. An estimated 28.2 % (95 % CI 19.0-36.6 %) of cases were attributable to rainfall above the recorded historical minimum. Conclusions: Rainfall is a robust, consistent predictor of leptospirosis incidence in the Dominican Republic, with the strongest association observed at a 1-month lag and a lag pattern broadly consistent with findings from distributed-lag studies in Thailand and the Philippines. These findings, which to our knowledge constitute the first formal quantification of this association for the insular Caribbean, provide an evidence base for rainfall-linked early-warning systems, with the strongest signal at approximately one month and elevated risk extending through three months after rainfall.

Mechanisms shaping population vulnerability to typhoon-related mortality remain poorly understood. Constructing a Bayesian spatio-temporal model, we linked 12.9 million deaths across Japan from 2010 to 2019 to population-weighted typhoon wind exposure and assessed effect modification by income, natural hazard vulnerability and healthcare access. Typhoon exposure was associated with 2,426 cumulative excess deaths [95% credible interval: 139, 4,632] among adults [&ge;]70 years, with mortality increasing within 0-1 weeks of exposure and more strongly in areas with limited healthcare access and greater hazard vulnerability. Among individuals <70 years, cumulative excess mortality was uncertain [781 deaths; -309 to 1,900], but delayed mortality increases were concentrated in lower-income and landslide-prone areas. These distinct patterns suggest that typhoon mortality reflects an interaction between acute exposure, demographic ageing and geographically uneven adaptive capacity, highlighting the need to incorporate local vulnerability into climate-resilient health systems.

Heritable bacterial symbionts are pervasive in terrestrial arthropods, often imposing reproductive manipulations to promote their own spread within host populations. Co-infections are common, potentially allowing symbiont co-infectors to hitchhike through a host population. However, adverse thermal conditions can disrupt these communities, particularly when co-infectors vary in their thermal sensitivity. We used a multi-generation experiment to test whether warm (29 {degrees}C) conditions disrupted spread of heritable symbionts through uninfected populations of the spider, Mermessus fradeorum. We tested two common infection combinations: a single infection with a cytoplasmic incompatibility (CI) inducing Rickettsiella or a feminizing co-infection that included a feminizing Wolbachia, the same Rickettsiella, and up to three apparent hitchhikers (two additional Wolbachia strains and Tisiphia). We initiated replicate populations with 1/3 of one infection type and 2/3 uninfected spiders, evaluating population infection rate over 5 spider generations under different temperature regimes. Under cool (21{degrees}C) conditions, Wolbachia feminization drove co-infection to 88% and Rickettsiella CI drove single infection to 83% of host populations. Vertical transmission for all symbionts was high (97-99%) and hitchhiking symbionts also spread effectively. Under warm conditions, feminization and CI efficacy were reduced, and symbionts suffered variably reduced vertical transmission. Warm conditions ultimately destroyed the co-infecting symbiont consortium and impeded symbiont spread. On its own, though, Rickettsiella was still able to increase, despite reduced strength of CI. We hypothesize that contrasting tensions between feminizing spread of the symbiont consortium versus environmentally driven loss of function and transmission may explain observed patterns of mixed infections in field populations of this spider.

Neighbourhood deprivation is one of the few potential policy-modifiable risk factors for psychiatric and neurological disorders, but the neurobiological pathways underlying these associations remain unclear. We investigated these relationships across three cohorts spanning the life span: the Healthy Brain and Child Development (HBCD) Study (n = 84, aged 0 to 4 weeks postnatal), the Adolescent Brain Cognitive Development (ABCD) Study (n = 4,792, aged 9 to 10 years), and the UK Biobank (UKB; approximately 500,000 adults, aged 44 to 87 years). Neighbourhood deprivation was associated with elevated disease risk, and individual lifestyle factors accounted for only a small fraction of this burden, indicating that the much larger residual effect reflects broader contextual characteristics of deprived environments rather than individual behaviours alone. Across all cohorts, greater deprivation consistently predicted lower cortical and subcortical brain volume, with effects detectable in early development and substantially stronger in adulthood. Across disorders, regional brain volume emerged as a consistent neuroanatomical mediator linking neighbourhood deprivation to neuropsychiatric disease. We further showed that deprivation preferentially affects brain regions intrinsically vulnerable to neuropsychiatric disorders. Spatial decoding analyses implicated dopaminergic and serotonergic neurotransmitter systems together with specific excitatory and inhibitory neuronal classes. Importantly, both the deprivation effects and their neuroanatomical mediation patterns were replicated across independent populations. Our study delivers a translational framework linking neighbourhood deprivation to brain health, which could inform public health policies and preventive interventions.

Most evidence of the consequences of climate change in natural systems has focussed on shifts in mean temperature (1,2), but the effects of extreme climatic events (ECEs) remain far less understood. This is particularly true for very severe ECEs that may occur only once every few decades. Understanding the consequences of these severe events for natural populations is nonetheless critical, since their frequency is predicted to rise under current climate change (3). Here we combine a unique long-term dataset spanning almost five decades of breeding (>20,000 events) and morphological data (>120,000 observations) in adult and nestling great tits (Parus major) and blue tits (Cyanistes caeruleus) with fine-scale temperature records to examine the effects of an unprecedented heatwave in May 2026 on breeding success and morphology. Average temperature during the heatwave (22-29 May 2026) was 7.85 C above the historical record, reaching +10.5 C (+4.32 SD) at its peak (25-26 May). These record-breaking temperatures significantly reduced adult breeding success and nestling bmass relative to expectation in the absence of a heat-wave. Given the heatwave was widespread (Fig. 1A), our findings from a single, exceptionally well-studied population are likely to generalise to other species exposed to the same event, providing key evidence that severe ECEs can substantially harm wild populations.