There is active interest in reconciling the tremendous variation observed in COVID-19 outcomes with host immunity. In this preprint, Sajuthi et al. analyse nasal airway epithelial transcriptomes from a large cohort of healthy and asthmatic subjects to distinguish relative contributions of host immune networks to coronavirus susceptibility. They use network co-expression analyses and transcriptomics on mucociliary cultures to show that genes implicated in SARS-CoV-2 infectivity, specifically TMPRSS2 and ACE2, are significantly influenced by type 2 cytokine-driven inflammation and interferon signalling, respectively. Although SARS-CoV-2-specific analysis and experiments are lacking, the study provides a rationale for why type 2 responses, which are aggravated in patients with asthma, might increase susceptibility to severe COVID-19.