IgA antibodies are enriched at mucosal surfaces and play an important role in host defense against viral pathogens. In addition to neutralizing viruses directly, antibodies can also engage specific receptors (Fc receptors) expressed on various immune-cell subsets to stimulate antimicrobial activities. While IgG Fc-mediated effector functions are known to mediate important antiviral activities, if and how IgA-mediated Fc-effector functions influence viral infections remains poorly understood. Here, we show that IgA–virus immune complexes stimulate neutrophils to undergo NETosis, a specific type of programmed cell death that results in release of chromatin studded with antimicrobial effector proteins. These neutrophil extracellular traps trap and inactivate viruses but can also have pathogenic consequences when poorly regulated.