Unravelling the size distribution of social groups with information theory on complex networks

The minimization of Fisher's information (MFI) approach of Frieden et al. [Phys. Rev. E {\bf 60} 48 (1999)] is applied to the study of size distributions in social groups on the basis of a recently established analogy between scale invariant systems and classical gases [arXiv:0908.0504]. Going beyond the ideal gas scenario is seen to be tantamount to simulating the interactions taking place in a network's competitive cluster growth process. We find a scaling rule that allows to classify the final cluster-size distributions using only one parameter that we call the competitiveness. Empirical city-size distributions and electoral results can be thus reproduced and classified according to this competitiveness, which also allows to correctly predict well-established assessments such as the "six-degrees of separation", which is shown here to be a direct consequence of the maximum number of stable social relationships that one person can maintain, known as Dunbar's number. Finally, we show that scaled city-size distributions of large countries follow the same universal distribution

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