Concurrent loss of ciliary genesWDR93andCFAP46in phylogenetically distant birds

Abstract

AbstractThe respiratory system is the primary route of infection for many contagious pathogens. Mucociliary clearance of inhaled pathogens is an important innate defense mechanism sustained by the rhythmic movement of epithelial cilia. To counter host defenses, viral pathogens target epithelial cells and cilia. For instance, the influenza virus modulates the expression ofWDR93, a central ciliary apparatus C1d projection component. Lineage-specific prevalence of such host defense genes results in differential susceptibility. Our comparative analysis of ∼500 vertebrate genomes supports the widespread conservation ofWDR93. However, we identified loss of theWDR93in landfowl, geese, and other phylogenetically-independent bird species. Notably, species withWDR93loss have concurrently lost another C1d component,CFAP46, through large segmental deletions. Understanding the consequences of such gene loss may provide insight into their role in host-pathogen interactions and benefit global pathogen surveillance efforts by prioritizing species missing host defense genes and identifying putative zoonotic reservoirs.