Type-III interferon, not type-I, is the predominant interferon induced by respiratory viruses in nasal epithelial cells.

摘要

As an innate immune response against diverse viral infections, a host induces two types of interferon (IFN), type-I (IFN-beta/alpha) and type-III (IFN-lambda). We investigated IFN inductions by respiratory viruses, including respiratory syncytial virus (RSV), measles virus and mumps virus in human nasal epithelial cells (NECs). IFN-lambda, but not IFN-beta/alpha, was induced by respiratory virus infection in primary NECs and immortalized NECs through transfection with the human telomerase reverse transcriptase gene (hTERT-NECs). In contrast, both IFN-lambda and IFN-beta/alpha were induced by RSV infection in human bronchiolar carcinoma cell line A549. Suppression of retinoic acid-inducible gene-I (RIG-I) expression using siRNA significantly reduced IFN-lambda1 production in RSV-infected hTERT-NECs, while suppression of melanoma differentiation-associated gene 5 (MDA5) expression did not. Exogenous IFN-lambda1 treatment suppressed RSV replication and chemokine induction in hTERT-NECs. These data indicate that IFN-lambda, but not IFN-beta/alpha, contributes to the main first line defense via RIG-I-dependent pathway against respiratory virus infection in NECs.