To study this, the team created lab-grown human nasal tissue from stem cells, producing structures that mimic the real nasal lining. This model included multiple cell types, such as mucus-producing cells and ciliated cells that help clear particles. “Since rhinovirus infects humans but not other animals, organotypic tissue models are especially valuable,” explained senior author Ellen Foxman.
The study revealed that interferons—proteins that block viral replication—play a central role. Nasal cells release interferons upon detecting the virus, activating antiviral defenses in both infected and neighboring healthy cells. Rapid interferon responses contained infections effectively, whereas blocking these responses allowed the virus to spread widely, causing extensive cell damage.
Researchers also observed that when viral growth exceeds early defenses, a separate pathway triggers excess mucus and inflammatory signals, contributing to airway inflammation and breathing difficulties. These mechanisms could offer targets for therapies that reduce symptoms while preserving antiviral defenses.
The model has limitations, as it lacks immune cells present in real infections. Future research will examine how these additional cells and environmental factors affect antiviral responses. First author Bao Wang noted that understanding the body’s defense mechanisms opens opportunities for novel therapeutics: “Our study highlights that how the body responds to a virus is critical in determining both whether illness occurs and its severity.”
REFERENCE: Bao Wang, Julien A.R. Amat, Valia T. Mihaylova, Yong Kong, Guilin Wang, Ellen F. Foxman. Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling. Cell Press Blue, 2026; 100001 DOI: 10.1016/j.cpblue.2025.100001
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