Pollen exposure significantly enhances the spread of coronavirus infections within the nasal lining by compromising antiviral immune responses. Research presented at the 2026 European Academy of Allergy and Clinical Immunology (EAACI) congress indicates that environmental allergens promote virus transmission between cells.
Scientists utilized a near-physiological model of human nasal epithelial cells from both allergic and non-allergic donors. After exposing these cells to birch and timothy grass pollen aerosols, researchers introduced human coronavirus 229E and SARS-CoV-2. The results showed a marked increase in infectious viral particle production following pollen pre-exposure.
The study identified a dual mechanism: pollen triggered sustained mucus production and ciliary activity while simultaneously suppressing key antiviral mediators like IL-29 and IFN-β. Concurrently, pro-inflammatory cytokines IL-6 and TSLP rose sharply. This shift impairs the epithelium's natural defense system while accelerating inflammatory pathways.
Molecular profiling revealed that pollen alters apoptosis and cellular stress response pathways. Unlike virus-only cultures where infection remained localized, pollen-exposed tissues exhibited widespread viral distribution. This suggests pollen facilitates cell-to-cell transmission, offering critical insight into why respiratory viral susceptibility spikes during high-pollen seasons.