Fig.1.

Potential mechanisms of RV-C infection in normal and asthmatic airway epithelium. We speculate, based on function of other cadherins, that CDHR3 could be preferentially localized on the cell surface within intercellular junctions. The CDHR3 genotype (rs6967330) that converts amino acid residue cysteine to tyrosine at position 529 (C₅₂₉→Y) leads to an increased cell surface expression of CDHR3. a. In a healthy intact epithelium with normal barrier function, CDHR3 is likely to be less accessible for RV-C binding resulting in a reduced infection and mild illness. b. Chronic allergic inflammation in asthmatic airways reduces epithelial barrier function, and this could secondarily increase accessibility of CDHR3 for RV-C binding in individuals with “asthma risk” genotype. As a result, RV-C could infect more cells, leading to more severe respiratory illness. Eos, eosinophils; ILC2, type 2 innate lymphoid cell.