Exploring the Bimodal Solar System via Sample Return from the Main Asteroid Belt: The Case for Revisiting Ceres

Abstract: Sample return from a main-belt asteroid has not yet been attempted, but appears technologically feasible. While the cost implications are significant, the scientific case for such a mission appears overwhelming. As suggested by the “Grand Tack” model, the structure of the main belt was likely forged during the earliest stages of Solar System evolution in response to migration of the giant planets. Returning samples from the main belt has the potential to test such planet migration models and the related geochemical and isotopic concept of a bimodal Solar System. Isotopic studies demonstrate distinct compositional differences between samples believed to be derived from the outer Solar System (CC or carbonaceous chondrite group) and those that are thought to be derived from the inner Solar System (NC or non-carbonaceous group). These two groups are separated on relevant isotopic variation diagrams by a clear compositional gap. The interface between these two regions appears to be broadly coincident with the present location of the asteroid belt, which contains material derived from both groups. The Hayabusa mission to near-Earth asteroid (NEA) (25143) Itokawa has shown what can be learned from a sample-return mission to an asteroid, even with a very small amount of sample. One scenario for main-belt sample return involves a spacecraft launching a projectile that strikes an object and flying through the debris cloud, which would potentially allow multiple bodies to be sampled if a number of projectiles are used on different asteroids. Another scenario is the more traditional method of landing on an asteroid to obtain the sample. A significant range of main-belt asteroids are available as targets for a sample-return mission and such a mission would represent a first step in mineralogically and isotopically mapping the asteroid belt. We argue that a sample-return mission to the asteroid belt does not necessarily have to return material from both the NC and CC groups to viably test the bimodal Solar System paradigm, as material from the NC group is already abundantly available for study. Instead, there is overwhelming evidence that we have a very incomplete suite of CC-related samples. Based on our analysis, we advocate a dedicated sample-return mission to the dwarf planet (1) Ceres as the best means of further exploring inherent Solar System variation. Ceres is an ice-rich world that may be a displaced trans-Neptunian object. We almost certainly do not have any meteorites that closely resemble material that would be brought back from Ceres. The rich heritage of data acquired by the Dawn mission makes a sample-return mission from Ceres logistically feasible at a realistic cost. No other potential main-belt target is capable of providing as much insight into the early Solar System as Ceres. Such a mission should be given the highest priority by the international scientific community

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