Mapping the interaction sites of human and avian influenza A viruses and complement factor H

• DOI: 10.3389/fimmu.2024.1352022
• Publication Date: 2024-04-18T10:57:57Z
• Authors: Iman Rabeeah; Elizabeth Billington; Béatrice Nal; Jean-Remy Sadeyen; Ansar A. Pathan; Munir Iqbal; Nigel J. Temperton; Peter F. Zipfel; Christine Skerka; Uday Kishore; Holly Shelton
• Keywords: Complement

The complement system is an innate immune mechanism against microbial infections. It involves a cascade of effector molecules that activated via classical, lectin and alternative pathways. Consequently, many pathogens bind to or incorporate in their structures host negative regulators the pathways as evasion mechanism. Factor H (FH) regulator pathway protects "self" cells from non-specific attack. FH has been shown viruses including human influenza A (IAVs). In addition its involvement regulation activation, also perform range functions on own direct interaction with pathogens. Here, we show can directly IAVs both avian origin, mediated IAV surface glycoprotein haemagglutinin (HA). HA bound common pathogen binding footprints structure, control protein modules, CCP 5-7 15-20. H1 H3 showed overlapped receptor site HAs, but footprint was more extensive for than HA. - impeded initial entry H1N1 H3N2 strains impact viral multicycle replication lung strain-specific. virus significantly inhibited by preincubation FH, whereas there no alteration replicative rate progeny release H1N1, H9N2 H5N3 strains. We have mapped between IAV, vivo significance which yet be elucidated.