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Publication Abstract from PubMed

SARS-CoV-2 respiratory-tract infection affects both vaccinated and unvaccinated persons suggesting factors besides adaptive immunity are operative. We investigated the role of collectin-11 (CL-11), an epithelial-secreted carbohydrate-binding lectin that drives innate immunity and eliminates pathogens by complement activation. SARS-CoV-2, despite binding CL-11 to activate complement, was resistant to lysis. Remarkably, opsonization by CL-11 enhanced virus production by infected respiratory epithelial cells independently of complement. Furthermore, infected cells expressing SARS-CoV-2 spike protein displayed enhanced vulnerability to CL-11 binding and membrane attack by complement. The mechanism of enhanced infectivity was ablated in the presence of L-fucose, which occupied the extended carbohydrate-binding cleft of CL-11 in a crystallographic analysis of complexes between L-fucose and CL-11. Our study suggests pathogenicity of SARS-CoV-2 is related to complement-resistance together with enhanced infectivity and injury of respiratory epithelial cells mediated by locally released CL-11.

Glycan recognition by collectin-11 drives SARS-CoV-2 infectivity and membrane injury of respiratory epithelial cells.,Polycarpou A, Wagner-Gamble T, Greenlaw R, O'Neill L, Kanabar V, Alrehaili A, Jeon Y, Baker J, Bafadhel M, Khan H, Malim MH, Romano M, Farrar CA, Smolarek D, Martinez-Nunez R, Doores KJ, Wallis R, Klavinskis LS, Sacks SH Proc Natl Acad Sci U S A. 2025 Oct 28;122(43):e2521209122. doi: , 10.1073/pnas.2521209122. Epub 2025 Oct 24. PMID:41134631^[1]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.