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An anthrax-causing agent, Bacillus cereus biovar anthracis , is a persistent and widespread cause of death for a broad range of mammalian hosts in a tropical rainforest, with important implications for the conservation of mammals such as chimpanzees. Anthrax threatens rainforest wildlife Anthrax is a disease that affects wildlife, livestock and humans, largely in low- and middle-income countries. To date, the disease has largely been studied in arid ecosystems, where outbreaks are commonly reported. Fabian Leendertz and colleagues study the dynamics of an anthrax-causing bacterium in a rainforest in Taï National Park, Ivory Coast, using mammal and fly samples collected over three decades. They find that anthrax is an important cause of mortality in diverse mammalian species, including chimpanzees, monkeys, duikers, mongooses and porcupines. Demographic modelling suggests that anthrax will speed up the decline of local chimpanzee populations, potentially leading to their extinction from the region. Anthrax is a globally important animal disease and zoonosis. Despite this, our current knowledge of anthrax ecology is largely limited to arid ecosystems, where outbreaks are most commonly reported 1 , 2 , 3 . Here we show that the dynamics of an anthrax-causing agent, Bacillus cereus biovar anthracis , in a tropical rainforest have severe consequences for local wildlife communities. Using data and samples collected over three decades, we show that rainforest anthrax is a persistent and widespread cause of death for a broad range of mammalian hosts. We predict that this pathogen will accelerate the decline and possibly result in the extirpation of local chimpanzee ( Pan troglodytes verus ) populations. We present the epidemiology of a cryptic pathogen and show that its presence has important implications for conservation.

The study of the archaeological remains of fossil hominins must rely on reconstructions to elucidate the behaviour that may have resulted in particular stone tools and their accumulation. Comparatively, stone tool use among living primates has illuminated behaviours that are also amenable to archaeological examination, permitting direct observations of the behaviour leading to artefacts and their assemblages to be incorporated. Here, we describe newly discovered stone tool-use behaviour and stone accumulation sites in wild chimpanzees reminiscent of human cairns. In addition to data from 17 mid- to long-term chimpanzee research sites, we sampled a further 34 Pan troglodytes communities. We found four populations in West Africa where chimpanzees habitually bang and throw rocks against trees, or toss them into tree cavities, resulting in conspicuous stone accumulations at these sites. This represents the first record of repeated observations of individual chimpanzees exhibiting stone tool use for a purpose other than extractive foraging at what appear to be targeted trees. The ritualized behavioural display and collection of artefacts at particular locations observed in chimpanzee accumulative stone throwing may have implications for the inferences that can be drawn from archaeological stone assemblages and the origins of ritual sites.

Human and simian immunodeficiency viruses (HIV/SIVs) use CD4 as the primary receptor to enter target cells. Here, we show that the chimpanzee CD4 is highly polymorphic, with nine coding variants present in wild populations, and that this diversity interferes with SIV envelope (Env)–CD4 interactions. Testing the replication fitness of SIVcpz strains in CD4⁺ T cells from captive chimpanzees, we found that certain viruses were unable to infect cells from certain hosts. These differences were recapitulated in CD4 transfection assays, which revealed a strong association between CD4 genotypes and SIVcpz infection phenotypes. The most striking differences were observed for three substitutions (Q25R, Q40R, and P68T), with P68T generating a second N-linked glycosylation site (N66) in addition to an invariant N32 encoded by all chimpanzee CD4 alleles. In silico modeling and site-directed mutagenesis identified charged residues at the CD4–Env interface and clashes between CD4- and Env-encoded glycans as mechanisms of inhibition. CD4 polymorphisms also reduced Env-mediated cell entry of monkey SIVs, which was dependent on at least one D1 domain glycan. CD4 allele frequencies varied among wild chimpanzees, with high diversity in all but the western subspecies, which appeared to have undergone a selective sweep. One allele was associated with lower SIVcpz prevalence rates in the wild. These results indicate that substitutions in the D1 domain of the chimpanzee CD4 can prevent SIV cell entry. Although some SIVcpz strains have adapted to utilize these variants, CD4 diversity is maintained, protecting chimpanzees against infection with SIVcpz and other SIVs to which they are exposed.

Even though information on global biodiversity trends becomes increasingly available, large taxonomic and spatial data gaps persist at the scale relevant to planning conservation interventions. This is because data collectors are hesitant to share data with global repositories due to workload, lack of incentives, and perceived risk of losing intellectual property rights. In contrast, due to greater conceptual and methodological proximity, taxon-specific database initiatives can provide more direct benefits to data collectors through research collaborations and shared authorship. The IUCN SSC Ape Populations, Environments and Surveys (A.P.E.S.) database was created in 2005 as a repository for data on great apes and other primate taxa. It aims to acquire field survey data and make different types of data accessible, and provide up-to-date species status information. To support the current update of the conservation action plan for western chimpanzees (Pan troglodytes verus) we compiled field surveys for this taxon from IUCN SSC A.P.E.S., 75% of which were unpublished. We used spatial modeling to infer total population size, range-wide density distribution, population connectivity and landscape-scale metrics. We estimated a total abundance of 52 800 (95% CI 17 577-96 564) western chimpanzees, of which only 17% occurred in national parks. We also found that 10% of chimpanzees live within 25 km of four multi-national 'development corridors' currently planned for West Africa. These large infrastructure projects aim to promote economic integration and agriculture expansion, but are likely to cause further habitat loss and reduce population connectivity. We close by demonstrating the wealth of conservation-relevant information derivable from a taxon-specific database like IUCN SSC A.P.E.S. and propose that a network of many more such databases could be created to provide the essential information to conservation that can neither be supplied by one-off projects nor by global repositories, and thus are highly complementary to existing initiatives.

Much like humans, chimpanzees occupy diverse habitats and exhibit extensive behavioural variability. However, chimpanzees are recognized as a discontinuous species, with four subspecies separated by historical geographic barriers. Nevertheless, their range-wide degree of genetic connectivity remains poorly resolved, mainly due to sampling limitations. By analyzing a geographically comprehensive sample set amplified at microsatellite markers that inform recent population history, we found that isolation by distance explains most of the range-wide genetic structure of chimpanzees. Furthermore, we did not identify spatial discontinuities corresponding with the recognized subspecies, suggesting that some of the subspecies-delineating geographic barriers were recently permeable to gene flow. Substantial range-wide genetic connectivity is consistent with the hypothesis that behavioural flexibility is a salient driver of chimpanzee responses to changing environmental conditions. Finally, our observation of strong local differentiation associated with recent anthropogenic pressures portends future loss of critical genetic diversity if habitat fragmentation and population isolation continue unabated.Lester and colleagues use faecal samples and genetic analyses to investigate the genetic connectivity across chimpanzees. Their results indicate that the global pattern of genetic diversity in chimpanzees is largely characterized by a pattern of isolation by distance with several isolated populations exhibiting strong local differentiation.

Gut microbial communities are drivers of primate physiology and health, but the factors that influence the gut microbiome in wild primate populations remain largely undetermined. We report data from a continent-wide survey of wild chimpanzee gut microbiota and highlight the effects of genetics, vegetation, and potentially even tool use at different spatial scales on the chimpanzee gut microbiome, including bacteria, archaea, and eukaryotic parasites. Understanding variation in host-associated microbial communities is important given the relevance of microbiomes to host physiology and health. Using 560 fecal samples collected from wild chimpanzees ( Pan troglodytes ) across their range, we assessed how geography, genetics, climate, vegetation, and diet relate to gut microbial community structure (prokaryotes, eukaryotic parasites) at multiple spatial scales. We observed a high degree of regional specificity in the microbiome composition, which was associated with host genetics, available plant foods, and potentially with cultural differences in tool use, which affect diet. Genetic differences drove community composition at large scales, while vegetation and potentially tool use drove within-region differences, likely due to their influence on diet. Unlike industrialized human populations in the United States, where regional differences in the gut microbiome are undetectable, chimpanzee gut microbiomes are far more variable across space, suggesting that technological developments have decoupled humans from their local environments, obscuring regional differences that could have been important during human evolution. IMPORTANCE Gut microbial communities are drivers of primate physiology and health, but the factors that influence the gut microbiome in wild primate populations remain largely undetermined. We report data from a continent-wide survey of wild chimpanzee gut microbiota and highlight the effects of genetics, vegetation, and potentially even tool use at different spatial scales on the chimpanzee gut microbiome, including bacteria, archaea, and eukaryotic parasites. Microbial community dissimilarity was strongly correlated with chimpanzee population genetic dissimilarity, and vegetation composition and consumption of algae, honey, nuts, and termites were potentially associated with additional divergence in microbial communities between sampling sites. Our results suggest that host genetics, geography, and climate play a far stronger role in structuring the gut microbiome in chimpanzees than in humans.

Aim: Paleoclimate reconstructions have enhanced our understanding of how past climates may have shaped present-day biodiversity. We hypothesize that habitat stability in historical Afrotropical refugia played a major role in the habitat suitability and persistence of chimpanzees (Pan troglodytes) during the late Quaternary. We aimed to build a dynamic model of changing habitat suitability for chimpanzees at finer spatio-temporal scales than previously available to provide a new resource for understanding their ecology, behaviour and evolution. Location: Afrotropics. Taxon: Chimpanzee (Pan troglodytes), including all four subspecies (P. t. verus, P. t. ellioti, P. t. troglodytes, P. t. schweinfurthii). Methods: We used downscaled bioclimatic variables representing monthly temperature and precipitation estimates, along with historical human population density data and an extensive database of georeferenced presence points to infer chimpanzee habitat suitability at 62 paleoclimatic time periods across the Afrotropics based on ensemble species distribution models. We map habitat stability over time using an approach that accounts for dispersal between time periods, and compare our modelled stability estimates to existing knowledge of Afrotropical refugia. Our models cover a spatial resolution of 0.0467 degrees (approximately 5.19 km2 grid cells) and a temporal resolution of every 1,000-4,000 years dating back to the the Last Interglacial (120,000 BP). Results: Our results show high habitat stability concordant with known historical forest refugia across Africa, but suggest that they are underestimated in their extent for chimpanzees. We provide the first fine-grained dynamic map of historical chimpanzee habitat suitability since the Last Interglacial which is suspected to have influenced a number of ecological-evolutionary processes, such as the emergence of complex patterns of behavioural and genetic diversity. Main Conclusions: We provide a novel resource that can be used to reveal spatio-temporally explicit insights into the role of refugia in determining chimpanzee behavioural, ecological and genetic diversity .This methodology can be applied to other taxonomic groups and geographic areas where sufficient data is available. Competing Interest Statement The authors have declared no competing interest. Footnotes * author affiliations updated

Analyses of tumour samples and tumour-infiltrating lymphocytes from two patients with melanoma who were treated with adoptive T-cell therapy provide evidence for tumour escape by loss and downregulation of immunogenic antigens. Tumour resistance to neoantigens A key question in the development of mutation-derived neoantigens as cancer immunotherapy is whether the neoantigen repertoire in human cancers will be stable when T-cell reactivity is elicited. Els Verdegaal et al . analyse sequential tumour samples and tumour-infiltrating lymphocytes from two patients with melanoma receiving adoptive T-cell therapy and provide evidence for tumour escape by loss and downregulation of immunogenic antigens. This result suggests that the therapeutic induction of broad neoantigen-specific T-cell responses should be used to avoid tumour resistance Recognition of neoantigens that are formed as a consequence of DNA damage is likely to form a major driving force behind the clinical activity of cancer immunotherapies such as T-cell checkpoint blockade and adoptive T-cell therapy 1 , 2 , 3 , 4 , 5 , 6 , 7 . Therefore, strategies to selectively enhance T-cell reactivity against genetically defined neoantigens 1 , 8 , 9 , 10 , 11 are currently under development. In mouse models, T-cell pressure can sculpt the antigenicity of tumours, resulting in the emergence of tumours that lack defined mutant antigens 12 , 13 . However, whether the T-cell-recognized neoantigen repertoire in human cancers is constant over time is unclear. Here we analyse the stability of neoantigen-specific T-cell responses and the antigens they recognize in two patients with stage IV melanoma treated by adoptive T-cell transfer. The T-cell-recognized neoantigens can be selectively lost from the tumour cell population, either by overall reduced expression of the genes or loss of the mutant alleles. Notably, loss of expression of T-cell-recognized neoantigens was accompanied by development of neoantigen-specific T-cell reactivity in tumour-infiltrating lymphocytes. These data demonstrate the dynamic interactions between cancer cells and T cells, which suggest that T cells mediate neoantigen immunoediting, and indicate that the therapeutic induction of broad neoantigen-specific T-cell responses should be used to avoid tumour resistance.

Ton Schumacher and colleagues show that melanoma patients have CD4+ T cells reactive to mutated tumor antigens. Tumor-specific neo-antigens that arise as a consequence of mutations 1 , 2 are thought to be important for the therapeutic efficacy of cancer immunotherapies 3 , 4 , 5 . Accumulating evidence suggests that neo-antigens may be commonly recognized by intratumoral CD8 + T cells 3 , 4 , 5 , 6 , 7 , but it is unclear whether neo-antigen–specific CD4 + T cells also frequently reside within human tumors. In view of the accepted role of tumor-specific CD4 + T-cell responses in tumor control 8 , 9 , 10 , we addressed whether neo-antigen–specific CD4 + T-cell reactivity is a common property in human melanoma.

Background Osteogenesis Imperfecta (OI) is a heritable connective tissue disorder mainly caused by mutations in the genes COL1A1 and COL1A2 and is associated with hearing loss in approximately half of the cases. The hearing impairment usually starts between the second and fourth decade of life as a conductive hearing loss, frequently evolving to mixed hearing loss thereafter. A minority of patients develop pure sensorineural hearing loss. The interindividual variability in the audiological characteristics of the hearing loss is unexplained. Methods With the purpose of evaluating inter- and intrafamilial variability, hearing was thorougly examined in 184 OI patients (type I: 154; type III: 4; type IV: 26), aged 3-89 years, with a mutation in either COL1A1 or COL1A2 and originating from 89 different families. Due to the adult onset of hearing loss in OI, correlations between the presence and/or characteristics of the hearing loss and the underlying mutation were investigated in a subsample of 114 OI patients from 64 different families who were older than 40 years of age or had developed hearing loss before the age of 40. Results Hearing loss was diagnosed in 48.4% of the total sample of OI ears with increasing prevalence in the older age groups. The predominant type was a mixed hearing loss (27.5%). A minority presented a pure conductive (8.4%) or pure sensorineural (12.5%) loss. In the subsample of 114 OI subjects, no association was found between the nature of the mutation in COL1A1 or COL1A2 genes and the occurrence, type or severity of hearing loss. Relatives originating from the same family differed in audiological features, which may partially be attributed to their dissimilar age. Conclusions Our study confirms that hearing loss in OI shows a strong intrafamilial variability. Additional modifications in other genes are assumed to be responsible for the expression of hearing loss in OI.