Disease risk and conservation implications of orangutan translocations

Critically Endangered orangutans are translocated in several situations: reintroduced into historic range where no wild populations exist, released to reinforce existing wild populations, and wild-to-wild translocated to remove individuals from potentially risky situations. Translocated orangutans exposed to human diseases, including Coronavirus Disease 2019 (COVID-19), pose risks to wild and previously released conspecifics. Wildlife disease risk experts recommended halting great ape translocations during the COVID-19 pandemic to minimize risk of disease transmission to wild populations. We collected data on orangutan releases and associated disease risk management in Indonesia during the COVID-19 pandemic, and developed a problem description for orangutan disease and conservation risks. We identified that at least 15 rehabilitated ex-captive and 27 wild captured orangutans were released during the study period. Identified disease risks included several wild-to-wild translocated orangutans in direct contact or proximity to humans without protective equipment, and formerly captive rehabilitated orangutans that have had long periods of contact and potential exposure to human diseases. While translocation practitioners typically employ mitigation measures to decrease disease transmission likelihood, these measures cannot eliminate all risk, and are not consistently applied. COVID-19 and other diseases of human origin can be transmitted to orangutans, which could have catastrophic impacts on wild orangutans, other susceptible fauna, and humans should disease transmission occur. We recommend stakeholders conduct a Disease Risk Analysis for orangutan translocation, and improve pathogen surveillance and mitigation measures to decrease the likelihood of potential outbreaks. We also suggest refocusing conservation efforts on alternatives to wild-to-wild translocation including mitigating human-orangutan interactions, enforcing laws and protecting orangutan habitats to conserve orangutans in situ

Disease Risk and Conservation Implications of Orangutan Translocations

Critically Endangered orangutans are translocated in several situations: reintroduced into historic range where no wild populations exist, released to reinforce existing wild populations, and wild-to-wild translocated to remove individuals from potentially risky situations. Translocated orangutans exposed to human diseases, including Coronavirus Disease 2019 (COVID-19), pose risks to wild and previously released conspecifics. Wildlife disease risk experts recommended halting great ape translocations during the COVID-19 pandemic to minimize risk of disease transmission to wild populations. We collected data on orangutan releases and associated disease risk management in Indonesia during the COVID-19 pandemic, and developed a problem description for orangutan disease and conservation risks. We identified that at least 15 rehabilitated ex-captive and 27 wild captured orangutans were released during the study period. Identified disease risks included several wild-to-wild translocated orangutans in direct contact or proximity to humans without protective equipment, and formerly captive rehabilitated orangutans that have had long periods of contact and potential exposure to human diseases. While translocation practitioners typically employ mitigation measures to decrease disease transmission likelihood, these measures cannot eliminate all risk, and are not consistently applied. COVID-19 and other diseases of human origin can be transmitted to orangutans, which could have catastrophic impacts on wild orangutans, other susceptible fauna, and humans should disease transmission occur. We recommend stakeholders conduct a Disease Risk Analysis for orangutan translocation, and improve pathogen surveillance and mitigation measures to decrease the likelihood of potential outbreaks. We also suggest refocusing conservation efforts on alternatives to wild-to-wild translocation including mitigating human-orangutan interactions, enforcing laws and protecting orangutan habitats to conserve orangutans in situ

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Disease Risk and Conservation Implications of Orangutan Translocations

Critically Endangered orangutans are translocated in several situations: reintroduced into historic range where no wild populations exist, released to reinforce existing wild populations, and wild-to-wild translocated to remove individuals from potentially risky situations. Translocated orangutans exposed to human diseases, including Coronavirus Disease 2019 (COVID-19), pose risks to wild and previously released conspecifics. Wildlife disease risk experts recommended halting great ape translocations during the COVID-19 pandemic to minimize risk of disease transmission to wild populations. We collected data on orangutan releases and associated disease risk management in Indonesia during the COVID-19 pandemic, and developed a problem description for orangutan disease and conservation risks. We identified that at least 15 rehabilitated ex-captive and 27 wild captured orangutans were released during the study period. Identified disease risks included several wild-to-wild translocated orangutans in direct contact or proximity to humans without protective equipment, and formerly captive rehabilitated orangutans that have had long periods of contact and potential exposure to human diseases. While translocation practitioners typically employ mitigation measures to decrease disease transmission likelihood, these measures cannot eliminate all risk, and are not consistently applied. COVID-19 and other diseases of human origin can be transmitted to orangutans, which could have catastrophic impacts on wild orangutans, other susceptible fauna, and humans should disease transmission occur. We recommend stakeholders conduct a Disease Risk Analysis for orangutan translocation, and improve pathogen surveillance and mitigation measures to decrease the likelihood of potential outbreaks. We also suggest refocusing conservation efforts on alternatives to wild-to-wild translocation including mitigating human-orangutan interactions, enforcing laws and protecting orangutan habitats to conserve orangutans in situ

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease