Galectin-3 exacerbates influenza a virus pathogenesis via dual mechanisms: Promoting hemagglutinin-dependent entry and driving nlrp3 inflammasome activation.
Gal3 is identified as a potent host factor that orchestrates excessive inflammation by simultaneously facilitating viral entry and driving the assembly of the NLRP3 inflammasome, highlighting the Gal3-NLRP3 axis as a promising therapeutic target to mitigate severe influenza-induced lung injury.