Incorporating prey demographics and predator social structure into prey selection and carrying capacity estimates for cheetah

There is a need for a refined understanding of large carnivore prey preference and carrying capacity (K). To date, K estimates for large carnivores have been developed from predictions of carnivore diet at a prey and predator species-level. These predictions therefore assume that all social classes within a carnivore species display similar prey preferences and that all demographic classes within a prey species are equally preferred or avoided. The objective of this study was to investigate the importance of including prey demographics and carnivore social class in carnivore diet descriptions and thereby K estimates, using cheetah Acinonyx jubatus as a study species. It was predicted that prey sex, prey age and cheetah social class influence cheetah prey preferences, when they influence the risk and ease of prey capture, and that their inclusion in a K model would improve its predictive strength. Based on an analysis of 1290 kills from South Africa, male coalition cheetah were found to prefer a broader weight range of prey than solitary cheetah. Prey demographics further influenced cheetah prey preference, when it corresponded to differences in prey size and the presence of horns. The current species-level K regression model for cheetah is based on preferred prey and thus omits highly abundant antelope that often comprise the majority of the diet, an artefact of the way in which preferences are calculated. A refinement of the species-level K regression model, to account for prey demographic- and cheetah social class-level differences in diet and the biomass of accessible prey (defined in this study as all non-avoided prey) instead of just preferred prey, doubled the predictive strength of the K model. Because group-hunting enabled predation on a broader weight range of prey, cheetah K was influenced by the ratio of male coalition cheetah to solitary cheetah in the population. The refined K regression model is derived from ecosystems supporting an intact carnivore guild. A mechanistic approach to estimating K, based on Caughley‟s (1977) maximum sustainable yield model, therefore better predicted cheetah K in systems devoid of lion Panthera leo and African wild dog Lycaon pictus, which were found to suppress cheetah density. This study improves our understanding of the relationships between prey demographics, cheetah social classes and intra-guild competition in determining cheetah prey preferences and K. This study therefore paves the way for similar work on other large carnivores

Consequences of recreational hunting for biodiversity conservation and livelihoods

The widespread activity of recreational hunting is proposed as a means of conserving nature and supporting livelihoods. However, recreational hunting-especially trophy hunting-has come under increasing scrutiny based on ethical concerns and the arguments that it can threaten species and fail to contribute meaningfully to local livelihoods. We provide an overview of the peer-reviewed literature on recreational hunting of terrestrial birds and mammals between 1953 and 2020 (> 1,000 papers). The most-studied species are large mammals from North America, Europe, and Africa. While there is extensive research on species' ecology to inform sustainable hunting practices, there is comparably little research on the role of local perceptions and institutions in determining socioeconomic and conservation outcomes. Evidence is lacking to answer the pressing questions of where and how hunting contributes to just and sustainable conservation efforts. We outline an agenda to build this evidence base through research that recognizes diverse social-ecological contexts.Peer reviewe

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Publisher Correction: Whole-genome sequencing of a sporadic primary immunodeficiency cohort (Nature, (2020), 583, 7814, (90-95), 10.1038/s41586-020-2265-1)

An amendment to this paper has been published and can be accessed via a link at the top of the paper