Evolution, Medicine, and Public Health

Parasitism is one of the key, structural, interspecific interactions in ecology. One remarkable parasitic strategy that has been documented in multiple systems is the behavioral manipulation of hosts to increase parasite fitness. While not yet documented in humans, we propose that a ubiquitous zoonotic parasite - Toxoplasma gondii - may change human behavior to favor the parasite by increasing the fitness of the parasites definitive host - cats. Specifically, we assess the possibility that human behavioral changes resulting from chronic, latent T. gondii infection lead to measurable changes in attitudes, actions and dopaminergic responses towards cats that function to increase domestic cat fitness. We assessed the potential role of humans in the T. gondii lifecycle by identifying and testing behavioral changes in humans that benefit the parasite; specifically, human affection for cats. We assessed T. gondii infection status in 68 participants using T. gondii serum antibody testing, and assessed their attitudes towards cats in three ways: i) surveys, ii) participant behavior in the presence of domestic cats, and iii) participant oxytocin levels before and after interactions with cats to assess dopaminergic changes. Only 2 of 68 participants were positive for T. gondii antibodies, limiting statistical power. However, our results indicated that T. gondii-positive participants both reported a greater affection for cats in surveys, and spent more time engaged with cats during behavioral trials than T. gondii-negative participants (87% of study time engaging with cats vs 75%). Oxytocin results were inconclusive.

Parental rejection of apparently healthy newborns is widely classified as a behavioural abnormality in captive primate colonies, yet its biological significance remains unclear. In owl monkeys (Aotus nancymaae), parental rejection, defined here as cessation of nursing leading to rescue nursery rearing, is typically lethal for offspring and is transmitted across generations despite reducing offspring survival. Here, we tested whether parental rejection is associated with lifespan and reproductive differences in parents and their surviving offspring. We analysed long-term demographic records from a captive colony of 962 individuals and compared survival and reproductive outcomes between rejector and non-rejector parents using survival analyses and regression-based models. Parents who rejected offspring lived significantly longer than non-rejectors, with an average lifespan advantage of approximately 4-4.5 years in both males and females. This survival difference was concentrated during the prime reproductive period (6-20 years). Well-reared offspring of rejector parents also lived longer than offspring of non-rejectors, with a mean lifespan difference of 1.26 years. Rejector parents produced more offspring overall, but this difference was explained by extended lifespan rather than higher reproductive output per year. Analyses stratified by rejection timing showed no longevity advantage in first-birth rejectors, whereas parents rejecting later-born offspring exhibited longer survival. Together, these findings show that parental rejection is associated with longer lifespan in parents and in their well-reared offspring under captive conditions. These patterns are consistent with altered allocation of parental investment under energetic or environmental stress.

Major surface antigens in many pathogens are encoded by rapidly diversifying multigene families, generating fitness variation through antigenic and functional differences. These variations align with the niche and absolute fitness axes of Modern Coexistence Theory (MCT). Yet, how such gene families evolve along these axes under competition for hosts and across transmission gradients remains poorly understood, as prior MCT studies have not explicitly accounted for evolutionary dynamics in high dimensions. We use a stochastic computational model of Plasmodium falciparum transmission to examine how transmission intensity and selection shape var multigene family evolution and composition within parasite genomes. Results show that selection alone cannot maintain the observed stable ratio of two gene groups within parasite genomes, indicating that group-based classifications do not clearly reflect transmission strategy or virulence. When a trade-off exists between diversification rates and absolute fitness, strong immune selection under high transmission favors fast-recombining genes while attenuating functional selection on R0-associated traits. In general, stronger immune selection increases the invasion probability of novel antigens and the niche differentiation among parasite genomes, while reducing the variance in gene-level transmissibility and expression duration, and therefore R0. This outcome, combining enhanced niche differentiation and reduced absolute fitness variation, departs from MCT predictions.

The expensive son hypothesis posits that mothers incur higher fitness costs when caring for sons versus daughters in species with male-biased size dimorphism. Evidence for maternal survival costs of sons in humans is limited to shortened overall lifespans; whether having more sons reduces short-term survival during reproductive years is unknown. Here, we utilised life-history data from 5,456 mothers from preindustrial Finland to examine whether mothers with more sons had reduced survival within one year of their last birth. While mothers with few children but more sons showed no differences in survival, at higher family sizes, mothers with more sons had increasingly lower survival. These differences peaked at [~]0.4% lower survival per son among mothers with five children, suggesting accumulated physiological costs of sons. These differences then declined and reversed among mothers with more children, potentially due to selective disappearance of frailer mothers. Our results suggest that studies focusing on post-menopausal mothers may bias estimates of the fitness costs of sons and reproductive costs more broadly. We recommend future research further examines the overlooked short-term fitness costs of sons during reproductive years, which is vital for understanding how life-history trade-offs, sexual dimorphism, and their interaction have shaped human evolution.

Hosts have evolved a variety of innate immune responses to pathogens. In many cases, hosts directly detect pathogen-associated molecular patterns (PAMPs) or pathogen effectors to trigger an immune response. However, hosts may also detect pathogens indirectly through guarding, whereby immune receptors monitor the effects of pathogens rather than the pathogens themselves. Guarding likely represents a more difficult evolutionary challenge for pathogens than direct recognition of PAMPs, as infection may require modifying or disrupting guarded host proteins. Recently, self-guarding has been discovered, in which the host target functions as both guard and guardee. Self-guarding appears to present an intractable problem for pathogens: modification of the host target may benefit replication, but also triggers an immune response. If self-guarding creates an apparently inescapable detection mechanism, why are most guarding systems composed of separate guards and guardees? Here, we use mathematical models of within-host pathogen and immune dynamics to compare guarding and self-guarding architectures. We show that self-guarding leads to a more rapid immune response and faster pathogen suppression, but is also more prone to false-positive immune responses, likely imposing greater costs through autoimmunity. We therefore hypothesise that the greater potential for false-positive immune responses may explain the relative scarcity of self-guarding.

A central question in Geroscience is whether early-life mortality, which declines from birth to sexual maturity, and late-life mortality, which grows exponentially in time, can be understood within a shared conceptual framework. We show that stochastic threshold models can explain both phases by incorporating heterogeneity in neonatal vulnerability. Using U.S. National Center for Health Statistics data, we find that infant mortality risk is strongly associated with neonatal clinical markers such as Apgar scores, gestational age, and birth weight, suggesting that initial physiological differences persist across early life. We show that the [~]1/t mortality decline generically arises in stochastic threshold models via depletion of the most vulnerable, across a wide range of model specifications. Incorporating this mechanism into the Saturating-Removal model captures both the early decline and the later Gompertz acceleration, reproducing the full J-shaped mortality curve. Together, our findings link neonatal vulnerability to late-life mortality dynamics within a shared stochastic framework, supporting a life-course perspective on aging and longevity.

Parasites can alter host populations in fundamentally different ways depending on whether exposure results in infection. Yet, most epidemiological and evolutionary inference focuses on established infections, leaving the fitness consequences of parasite exposure comparatively understudied. This gap is consequential because hosts are frequently exposed to diverse parasite genotypes, and these encounters can impose substantial fitness costs even when infection does not occur. Theory predicts that hosts may mitigate these costs when interacting with commonly encountered parasite genotypes, such that exposure to sympatric parasites incurs lower fitness consequences than exposure to novel, allopatric parasites. Here, we examine the fitness consequences of exposure and infection in the first intermediate host of the trophically transmitted tapeworm Schistocephalus solidus, a cyclopoid copepod that serves as the first host in a three-host life cycle. Using sympatric (Vancouver Island, Canada) and allopatric (Norway) host-parasite combinations, we found a striking reciprocal asymmetry. Sympatric parasites were significantly more infective, yet exposure to sympatric parasites imposed weaker fitness costs when infection did not establish. In contrast, allopatric parasites were less infective, but exposed females produced fewer eggs and had lower hatching success than both controls and females exposed to sympatric parasites, indicating substantial genotype-dependent costs of exposure. Moreover, we found that infection was highly virulent across all genotypes: a single parasite caused near-complete reproductive suppression and reduced host survival across all host-parasite pairings, confirming S. solidus as a castrating parasite in copepods. Together, these results demonstrate that exposure, not just infection, acts as a critical ecological filter with potentially large and underappreciated consequences for host population dynamics and parasite transmission.

Evolution of drug resistance to one drug can alter the minimum inhibitory concentration to another drug. This phenomenon, known as a collateral effect, can manifest as either cross-resistance or collateral sensitivity. Various patterns of collateral effects have been observed experimentally. Repeated adaptation from the same parental strain may result in variable collateral effects; this is non-repeatability. Additionally, adaptation of a pathogen to one drug may produce a specific collateral effect to a second drug, while altering the order of drug exposure can result in a different, or even absent, collateral effect. This phenomenon is termed unidirectionality. The genetic and evolutionary mechanisms underlying these patterns remain incompletely characterised. Here, we propose a frame-work that integrates pharmacodynamics and population genetics and provide minimal examples to explain these patterns and their combinations. Furthermore, we demonstrate that drug concentration and selection regime strongly influence patterns of collateral effects, including repeatability, directionality, and their temporal dynamics.

Influenza infection results from tightly coupled interactions between viral replication, host immune responses, and the emergence of clinical symptoms. While mathematical models have extensively characterized viral and immune dynamics, the mechanistic link between immune activity and disease severity remains poorly understood. Here, we develop an integrative within-host modeling framework that explicitly connects infection dynamics, immune responses, and symptom manifestation through a unified dynamical system. Using murine influenza data, we incorporate key immune components alongside a mechanistic representation of symptom progression, quantified via host weight loss. Our analysis identifies inflammatory signaling, particularly TNF--mediated pathways, as a central driver linking immune activity to symptom severity. Importantly, we demonstrate that age-dependent alterations in immune regulation reshape this coupling: aged hosts exhibit prolonged inflammatory responses that amplify and sustain symptom burden despite comparable viral kinetics. These results highlight that disease severity cannot be inferred from viral load alone, but instead emerges from the dynamical interplay between immune regulation and host physiology. This framework provides a quantitative basis for understanding age-specific morbidity and offers a foundation for designing interventions that target immune-mediated pathology rather than viral replication alone.

ObjectiveStudies of nutritional status and host responses during severe and critical illness have focused predominantly on obesity; in contrast, the relationship between undernutrition, host responses, and clinical outcomes in adults hospitalized with severe infection remains poorly defined. We sought to determine whether severe undernutrition is associated with distinct host responses and clinical outcomes in adults hospitalized with severe infection. DesignProspective cohort study. SettingTwo public referral hospitals in Uganda. PatientsNon-pregnant adults ([≥]18 yr) hospitalized with severe, undifferentiated infection. InterventionsNone. Measurements and Main ResultsWe analyzed clinical data and serum Olink proteomic data from 432 participants (median age, 45 yr [IQR, 31-57 yr]; 44% male). Overall, 213 participants (49%) met prespecified criteria for undernutrition, including 52 (12%) with severe undernutrition. Clinically, severe undernutrition was associated with HIV coinfection, microbiologically diagnosed tuberculosis, greater physiological instability, and higher mortality. After adjustment for age, sex, illness duration, study site, and HIV, malaria, and tuberculosis coinfection, severe undernutrition was associated with higher expression of proteins involved in pro-inflammatory immune signaling, endothelial and vascular remodeling, hypoxia and oxidative stress responses, and extracellular matrix remodeling, together with lower expression of proteins linked to growth signaling, anticoagulant regulation, and lipid homeostasis. ConclusionsSevere undernutrition is associated with a distinct high-risk clinical phenotype and biologic signature in adults hospitalized with severe infection. These findings suggest that undernutrition may potentiate key domains of sepsis pathobiology, with implications for strengthening nutritional support and informing host-directed treatment strategies in low- and middle-income countries where malnutrition is common. Key PointsO_ST_ABSQuestionC_ST_ABSHow does undernutrition influence immune, metabolic, and endothelial responses to severe infection in adults? FindingsIn this multicenter cohort study of 432 adults hospitalized with severe infection in Uganda, severe undernutrition was associated with greater physiologic instability, higher mortality, and a distinct proteomic host-response profile. Adults with severe undernutrition exhibited a proteomic signature characterized by pro-inflammatory immune signaling, endothelial and extracellular matrix remodeling, and hypoxia and oxidative stress responses, together with lower expression of proteins involved in growth signaling, anticoagulant regulation, and lipid homeostasis. MeaningSevere undernutrition is associated with a distinct high-risk clinical and biologic phenotype during severe infection, with implications for nutritional support, risk stratification, and host-directed therapeutic strategies, particularly in low- and middle-income countries.

While SARS-CoV-2 and influenza continue to place a significant burden on population health, within-household differences in decisions towards vaccination and seeking care across these two pathogens, and across sociodemographic groups, remain largely unexplored. By conducting a household-level survey in Illinois, we found that many individuals made inconsistent decisions about vaccination: among all adults, 29% were vaccinated for only one of COVID-19 or influenza, and among those with children in the home, 39% lived with a child whose influenza or COVID-19 vaccination status differed from their own. A higher proportion of adults were vaccinated against COVID-19 compared to influenza, while the opposite was true for those younger than 18 years old. These differences hold even when accounting for disparities in coverage by age, race/ethnicity, political affiliation, and socioeconomic status. While vaccinated individuals consistently reported wanting to protect themselves or others, those who declined vaccination reported highly heterogeneous reasons ranging from resource constraints to distrust or misconceptions about vaccination. These differences are even more pronounced for COVID-19, with larger partisan gaps and higher refusal driven by safety concerns, lack of trust, or religious reasons than those who decide not to get the influenza vaccine. In contrast to vaccination, the decision to seek medical care when sick showed opposite sociodemographic trends, that are likely attributable to illness severity. Our findings highlight that closing gaps in COVID-19 and influenza vaccination coverage will require an integrative strategy that accounts for diverse motivations, fears, and barriers to access, while addressing social inequalities common to both diseases.

Background: Wearing facemasks and practising social distancing slow the spread of respiratory pathogens. However, in the event of a new pandemic emerging, the willingness of populations to voluntarily adopt these behaviours is unclear. Methods: A discrete choice experiment was conducted among 2,006 UK-based adults. Participants were presented with hypothetical scenarios describing the emergence of a respiratory virus pandemic and were asked to choose when they would wear facemasks and practise social distancing. A mixed multinomial logit model was used to jointly estimate how disease severity and prevalence, uncertainty in these quantities, and individual-level characteristics influence behavioural choices. Findings: Participants were averse to facemasks and social distancing in the absence of pandemic risk. For each ten-unit increase in severity (10 additional hospitalisations/1,000 infections), the odds of always wearing a facemask outside the home increased by 15.9% (95%CI: 14.3%, 17.5%), relative to rarely/never, and the odds of avoiding all people as much as possible increased by 16.4% (14.6%, 18.2%), relative to not avoiding anyone. Greater disease prevalence, uncertainty in disease severity or disease prevalence, a university education, prior COVID-19 vaccination and non-white ethnicity were also associated with choosing to always wear facemasks and avoid all people as much as possible. The probability of participants choosing to rarely/never wear facemasks varied from 13.4% (11.9%, 14.9%) in the lowest-risk scenario to 1.4% (1.2%, 1.7%) in the highest-risk scenario. Interpretation: Perceived risks of disease and associated uncertainty drive intention of UK adults to adapt their behaviour in a future pandemic.

End of life is characterized by a phase of rapid physiological decline and high morbidity, phenotypically observed as the "Smurf" phase in Drosophila, metabolic end-of-life dysregulation in mice, and end-stage frailty in humans. Existing two-phase aging models often conceptualize this end-of-life phase as a discrete biological state. Here, we demonstrate that a continuous stochastic model of damage accumulation, the saturating removal (SR) model, captures these multi-species morbidity dynamics. By defining the end-of-life phase as a stochastic crossing of a sub-lethal damage threshold, the SR model accurately reproduces empirical end-of-life dynamics across flies, mice, and humans. The model predicts a surprising temporary reduction in hazard shortly after entering the end-of-life phase, resulting in a U-shaped hazard curve, consistent with the empirical data in all three organisms. It also correctly predicts a shortening twilight phenomenon where the mean duration of the end-of-life phase decreases the later its onset. We conclude that end-of-life dynamics are consistent with universal features of a driver of aging crossing a threshold for end-of-life morbidity and then a threshold for death.

A quarter of the world's population has immunologic evidence of past or present Mycobacterium tuberculosis (Mtb) infection (MTBI) detected as TST or IGRA positivity. Community-based preventive treatment of individuals with MTBI has resulted in transient decreases in TB cases, but its long-term effectiveness has been controversial. Due to the likelihood that many of those with immune responses to Mtb antigens may no longer harbor Mtb, widespread treatment of all such individuals may result in unnecessary exposure to antibiotics. We raise an additional concern that preventive treatment of individuals with MTBI, who are not at the risk of disease progression, may result in loss of protective immunity, provided by the persistent infection, and enhanced risk of TB upon re-exposure to Mtb. There is evidence from human cohorts and animal studies that prior exposure to Mtb confers protection against TB development upon re-exposure, and that treatment of Mtb-infected animals often results in loss of this protection. We build a novel epidemiological model of Mtb dynamics and progression to TB in a community allowing for protection afforded by MTBI against exogenous reinfection-driven disease progression. We show that implementation of treatment of MTBI in the whole community will result in reduction of TB cases but stopping the program may result in an increase in new TB cases that may offset (or even exceed) benefits of the preventive treatment program. Our results suggest that better understanding protective effects provided by MTBI against progression to TB upon Mtb re-exposure and identification of Mtb-infected individuals who most benefit from preventive treatment must be a priority before preventive treatment of asymptomatic MTBI is widely implemented.

Research on under-vaccination often segments populations using demographic or administrative variables that are operationally useful but fail to capture identity dimensions relevant to vaccination decisions. Drawing on social identity theory, we propose an identity-landscape approach distinguishing identity membership, identity centrality, and multidimensional identity structure. Using a cross-sectional survey of 1,000 UK parents, we measured 65 identity indicators, identity-importance ratings, and their association with attitudinal and behavioural hesitancy toward childhood vaccination using validated scales. Beyond established socio-demographic predictors, alternative-medicine and natural-lifestyle identities, as well as affiliation with social media networks, were linked to greater hesitancy. Greater centrality of religion and political affiliation within personal identity was also associated with higher hesitancy. Principal component analysis suggested that individuals actively engaged across multiple societal issues were more hesitant, whereas stereotypically male-gendered engagement was associated with lower hesitancy. An identity-focused population segmentation may identify previously unrecognized undervaccinated groups and inform innovative tailored immunization campaigns.

The Red Queen Hypothesis proposes that genetic variation is maintained in populations through antagonistic coevolution of hosts and parasites. A major assumption of the Red Queen Hypothesis is tight genetic specificity for infection. However, it has been argued that this genetic interaction of host and parasite (GHxGP) is sensitive to environmental context (GHxGPxE). Environmental change could accordingly disrupt coevolutionary oscillations on relevant time scales, calling into question antagonistic coevolution as a general and robust explanation for the maintenance of genetic diversity. To evaluate this critique, we used the plant-parasitic nematode Meloidogyne arenaria and its natural bacterial parasite Pasteuria penetrans to determine if specificity is altered by temperature. We exposed six isofemale host lines to five parasite sources at three ecologically relevant temperatures. We found that, at two of three temperatures, susceptibility to infection depended on the specific combination of host line and parasite source (GHxGP). This specificity varied across temperatures, consistent with a GHxGPxE effect. This three-way interaction was driven both by quantitative changes in the strength of specificity across temperatures and shifts in the susceptibility rankings of host-parasite combinations. Our study contributes a rare experimental test of a proposed challenge to the Red Queen Hypothesis and suggests the potential for environmental context to change host-parasite specificity.

The COVID-19 pandemic saw successive emergence and global spread of novel viral variants, exhibiting enhanced transmissibility or evasion of immunity. While the genotypic and phenotypic basis of SARS-CoV-2 variants have been extensively characterized, the evolutionary factors governing their patterns of emergence are less well understood. In this study we systematically investigated how the invasion dynamics of viral variants depend on variant phenotype (increased transmissibility or immune evasion), source (local evolution vs importation), the timing of introduction, the distribution of population susceptibility, and the contact network structure. Using a stochastic multi-strain epidemic model, we find that strains with only a transmission advantage are more likely to emerge earlier in the epidemic, and rapidly and predictably dominate the viral population. In contrast, immune-escape variants tend to linger at low prevalence for extended time periods after emergence, avoiding detection, until a critical amount of immunity has built up in the population and they begin to rapidly outcompete existing strains. We find that two common features of realistic human contact networks---heterogeneity in contacts (overdispersion) and clustering---lead to more punctuated evolutionary dynamics. This work provides insight into past dynamics of SARS-CoV-2 variants and can help define planning scenarios for future epidemic modeling efforts.

This study explores the proximal and biological mechanisms underlying male same-sex orientation, with a focus on the Fraternal Birth Order Effect (FBOE), a robust phenomenon whereby androphilic men tend to have more older brothers, and its relationship with the Sororal Birth Order Effect (SBOE), whereby older sisters also appear to influence sexual orientation, albeit less consistently. The Maternal Immune Hypothesis (MIH), which posits that maternal immune responses to male-specific antigens accumulate across successive male pregnancies, provides a compelling proximal explanation for the FBOE, but it fails to fully account for the SBOE and other birth order patterns, such as the elevated prevalence of same-sex orientation among only-children compared to firstborns in larger sibships. Through explicit modelling of the MIH, our simulations reveal that the correlation between the number of older brothers and sisters generates a spurious SBOE, which disappears when controlling for older brothers, unless miscarriages are considered, in which case this control becomes insufficient. Additionally, the increased prevalence of same-sex orientation among only-children, relative to firstborns with siblings, only emerges when miscarriages are incorporated into the model. Empirical analyses across eight diverse populations (Indonesia, France, French Polynesia, Greece, Canada, Czech Republic, Samoa, Iran) confirm the presence of an overall significant FBOE and, critically, an overall significant SBOE even after controlling for the number of older brothers. The higher frequency of same-sex orientation men among only-children, compared to firstborns in larger sibships, further supports a possible role of miscarriage. However, the miscarriage rates estimated to explain the observed SBOE (37% - 57%) exceed typical reported rates (10% - 30%), suggesting either that additional mechanisms contribute to a spurious SBOE or that a non-spurious SBOE exists alongside the FBOE. Limitations of this study are discussed, as well as whether the MIH framework can be extended to accommodate these findings, or if alternative explanations are needed to resolve these discrepancies.

Haemosporida is a diverse order of vector-borne apicomplexan parasites infecting terrestrial vertebrates worldwide, including humans, but the evolutionary relationships among its genera remain unresolved. The phylogenetic placement of two bat-restricted genera, Nycteria and Polychromophilus, both of which lack erythrocytic schizogony, has varied across studies depending on taxon sampling and marker choice. To address this problem, an expanded dataset of near-complete mitochondrial (mtDNA) genomes together with nine nuclear loci were analyzed. Phylogenetic analyses of mtDNA recovered Nycteria and Polychromophilus as a strongly supported monophyletic clade. In contrast, analyses based only on the three mitochondrial coding genes (CDS) or a reduced nuclear dataset failed to recover their monophyly and showed low support and extensive topological conflict at deeper nodes. These results indicate that near-complete mitochondrial genomes recover phylogenetic signal that is not captured by reduced mitochondrial coding sequences or partial nuclear datasets. Molecular dating analyses further showed that divergence estimates for a putative Nycteria-Polychromophilus clade are compatible with the proposed times for bats diversification, and consistent with the broader haemosporidian timescale. When the Nycteria-Polychromophilus clade was incorporated as a calibration prior, divergence-time estimates became more precise without altering the overall evolutionary timeframe. Substantial mitochondrial gene-order rearrangements in a distinct Nycteria lineage were confirmed, highlighting structural divergence within this bat-associated group. In addition, heterogeneity in rates across mtDNA haemosporidian lineages was observed. Together, these findings support the existence of a distinct bat-associated clade whose deeper placement and evolutionary significance should be tested with broader phylogenomic sampling. Author SummaryMalaria parasites belong to a diverse group of organisms that infect many kinds of vertebrates, including birds, reptiles, and mammals (such as humans). Understanding how these parasites are related to each other is important for explaining how key biological traits have evolved. However, the relationships among major groups of haemosporidian parasites, including malaria parasites, remain unclear, particularly for those infecting bats. In this study, we focused on two groups of bat parasites, Nycteria and Polychromophilus, which share unusual biological features. The inferred evolutionary relationships of these two genera to other haemosporidians have been inconsistent across previous studies. By analyzing near-complete mitochondrial genomes, we found strong evidence that these two groups descended from a common evolutionary ancestor. In contrast, smaller datasets including nuclear genes failed to recover this relationship and produced conflicting results, suggesting that they lack sufficient information to resolve deep evolutionary relationships. We also found that this bat-associated lineage likely originated around the same time as early bats. In addition, we identified structural changes in the mitochondrial genome of one lineage, highlighting its evolutionary distinctiveness. Together, our results suggest that bats host a unique group of malaria parasites and demonstrate that more complete genetic data are essential for resolving their evolutionary history.

Object play - seemingly non-functional interactions with objects - can promote the development of foraging skills, tool use, and behavioral innovation. Among Catarrhine monkeys, it was described in macaques and baboons. Wild geladas, although closely related to baboons, have been described as lacking object play (observed only in captivity) linked to their specialized grazing ecology. Here, we provide the first evidence of both social and solitary object play in a wild gelada population (NOMUs=13) at Debre Libanos (Ethiopia) and compare it with object play in sympatric olive baboons (Nindividuals=42). Notably, immature geladas engaged in object play both socially and solitarily, but the latter case was most frequent also with novel objects introduced by researchers. Solitary object play occurred at levels comparable to those of baboons, challenging previous reports of limited object interest in geladas. This finding aligns with the occurrence of object play in phylogenetically related species and with the retention in wild geladas of arboreal behavior and fruit consumption and hand morphology enhancing fine manipulation. Hence, object play in geladas under certain environmental conditions may reflect a biologically rooted capacity and underscores the importance of ecological variability, as distinct behavioral ecotypes can emerge across different populations of the same species.