Transcriptomic profiling of PBMCs indicated that acutely infected participants who subsequently developed LC had higher levels of proinflammatory pathways such as IFNβ and IFNγ, JAK-STAT and IL-6 signaling, as well as innate immune cell signatures of monocytes neutrophils and complement and coagulation cascades (CCL3, CCL20, CD160, F13A1, F3, IL6, NR4A1, NLRP3, THBS1) during acute infection compared with acutely infected patients who fully recovered (CCs) (Extended Data Fig. 4a,b). This evidence concerns the gene IFNB1 and laryngotracheoesophageal cleft.