SARS-CoV-2 Infection of Human Lung Air-Liquid Interface Cultures Reveals Basal Cells as Relevant Targets.

Summary

Using primary human nasal/bronchial air–liquid interface cultures, SARS-CoV-2 (WT and Alpha) robustly infects basal cells, which substantially shape epithelial immune responses. Local camostat mesylate reduces viral load and immune activation in both basal and apical compartments.

Key Findings

• Basal cells are strongly infected by SARS-CoV-2 (WT and Alpha) alongside ciliated and secretory cells.
• Basal cells significantly contribute to epithelial immune responses in a donor-specific manner.
• Topical camostat mesylate reduces viral load and immune activation in both basal and apical compartments.

Clinical Implications

Supports evaluating topical camostat for early upper-airway SARS-CoV-2 infection and guides epithelial cell-type–specific strategies for prophylaxis and treatment.

Limitations

• In vitro epithelial models may not fully recapitulate in vivo immune and tissue dynamics.
• Therapeutic findings with camostat are preclinical; clinical efficacy remains to be established.

Future Directions

Clinical trials of intranasal camostat; define basal cell-specific antiviral pathways and interactions with ciliated/secretory cells in vivo.