Overview
- Researchers at Yale grew air-exposed human nasal organoids containing mucus-producing and ciliated cells to model early infection dynamics.
- Epithelial interferons established an antiviral state that curbed viral replication even in the absence of recruited immune cells.
- Blocking interferon signaling led to higher viral loads, broad infection of ciliated cells, tissue injury, and in some cases death of the organoids.
- When antiviral control waned, alternate sensing pathways drove mucus overproduction and heightened inflammation, pointing to host-directed therapeutic targets.
- Published January 19 in Cell Press Blue, the study charted a two-day surge in interferon-response genes before tapering and called for follow-up in models with additional cell types and in vivo settings.