Differential host responses by the type I and III interferons in primary differentiated human nasal epithelial cells are a determinant of antiviral activity

Background

The interferon (IFN) response is a crucial innate antiviral defence mechanism at the airway epithelium. The epithelial IFN response is predominantly mediated by the type I (IFN-β1) and III (IFN-λ) IFNs, which activate a transcriptional program expressing antiviral and inflammatory genes. Type III IFNs have been purported to be less inflammatory than type I IFN, but exhibit reduced potency. As both type I and III IFNs exert broad antiviral functions, there has been considerable interest in harnessing them as antiviral therapeutics. A better understanding of the effects of exogenous IFN on the host may enable its safer utilisation and prevent unwanted effects in clinical settings. Few studies have compared their potency using a standardised concentration or on primary human cells.