Entering the Innovation Twilight Zone: How Patent and Antitrust Law Must Work Together

Patent law and antitrust law have traded ascendancy over the last century, as courts and other institutions have tended to favor one at the expense of the other. In this Article, we take several steps toward stabilizing the doctrine surrounding these two branches of law. First, we argue that an optimal balance between patent rights and antitrust enforcement exists that will maximize consumer welfare, including promoting innovation and economic growth. Further, as Congress is the best institution to find this optimum, courts should enforce both statutes according to their literal text, which grants absolute patent rights but allows for more discretion in antitrust enforcement. Second, we propose three possible reasons for the historical conflict between these regimes: cultural cognition, political economy, and federal court structure. As a result, we propose two stabilizing solutions: research into culturally depolarizing communication techniques and a two-court Innovation Circuit

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