However, our data indicate a strong correlation between levels of infectious viral particles released into the apical wash and gene expression of IFNB1, IFNL1 and several ISGs following infection with either SARS-CoV-2 or H1N1, suggesting that reduced ability of SARS-CoV-2 to replicate in bronchial epithelial cells, rather than its evasion strategies, is the major driver for the delayed interferon response at transcriptional level. The gene discussed is IFNL1; the disease is infection.