Impacts of climate change on national biodiversity population trends

Climate change has had well-documented impacts on the distribution and phenology of species across many taxa, but impacts on species’ abundance, which relates closely to extinction risk and ecosystem function, have not been assessed across taxa. In the most comprehensive multi-taxa comparison to date, we modelled variation in national population indices of 501 mammal, bird, aphid, butterfly and moth species as a function of annual variation in weather variables, which through time allowed us to identify a component of species’ population growth that can be associated with post-1970s climate trends. We found evidence that these climate trends have significantly affected population trends of 15.8% of species, including eight with extreme (> 30% decline per decade) negative trends consistent with detrimental impacts of climate change. The modelled effect of climate change could explain 48% of the significant across-species population decline in moths and 63% of the population increase in winged aphids. The other taxa did not have significant across-species population trends or consistent climate change responses. Population declines in species of conservation concern were linked to both climatic and non-climatic factors respectively accounting for 42 and 58% of the decline. Evident differential impacts of climate change between trophic levels may signal the potential for future ecosystem disruption. Climate change has therefore already driven large-scale population changes of some species, had significant impacts on the overall abundance of some key invertebrate groups and may already have altered biological communities and ecosystems in Great Britain

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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