POLLEN exposure may enhance the spread of coronavirus infections within the nasal lining by weakening antiviral immune responses and promoting virus transmission between cells, according to research presented at the 2026 annual congress of the European Academy of Allergy and Clinical Immunology.
Previous laboratory and epidemiological studies have suggested that pollen exposure may increase susceptibility to respiratory viral infections, including rhinovirus and SARS-CoV-2. To investigate the underlying mechanisms, researchers used a near-physiological in vitro model of differentiated human nasal epithelial cells to examine how exposure to birch and timothy grass pollen aerosols influenced subsequent coronavirus infection.
Pollen Exposure Increases Coronavirus Spread in Nasal Cells
Human nasal epithelial cells derived from allergic and non-allergic donors were cultured at the air–liquid interface and exposed to pollen aerosols before infection with either human coronavirus 229E (hCoV-229E) or SARS-CoV-2. Viral replication was assessed using plaque assays, while cytokine production, proteomic changes, and spatial transcriptomic profiles were also analysed.
Exposure to pollen aerosols induced marked mucus production and coordinated ciliary activity that persisted for up to 72 hours. Importantly, pre-exposure to both birch and grass pollen significantly increased the production of infectious viral particles following infection with hCoV-229E and SARS-CoV-2. Researchers also observed reduced levels of the antiviral mediators IL-29 and IFN-β, alongside increased concentrations of the pro-inflammatory cytokines IL-6 and thymic stromal lymphopoietin (TSLP), compared with virus-only controls. These findings suggest that pollen exposure may impair the epithelial antiviral response while simultaneously promoting inflammatory pathways.
Altered Immune and Stress Pathways May Drive Viral Transmission
Further molecular analyses provided insight into the mechanisms underlying these effects. Proteomic profiling of cells co-exposed to birch pollen and hCoV-229E revealed enrichment of pathways associated with apoptosis, cellular stress responses, and cAMP- and MAPK-mediated signalling. Spatial transcriptomic analysis showed that, in virus-only cultures, high levels of viral gene expression were largely confined to a small number of infected ciliated cells. In contrast, pollen-pre-exposed cultures exhibited lower viral gene expression within individual infected cells but a much broader distribution of infection throughout the tissue.
The authors concluded that pollen exposure may facilitate cell-to-cell transmission of coronaviruses within the nasal epithelium by altering stress response and apoptosis-regulating pathways. These findings provide further evidence that environmental pollen exposure can influence host antiviral defences and may contribute to increased susceptibility to respiratory viral infections.
Reference
Eggestein A et al. Exposure of nasal epithelial cells with pollen aerosols and coronaviruses in a near-physiological in vitro model. Abstract 100340. EAACI, 12-15 June, 2026.
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