Human neutrophil respiratory burst response to influenza A virus occurs at an intracellular location.

We have studied in detail the in vitro interactions of influenza A viruses (IAVs) with human neutrophils to clarify why these cells become dysfunctional during IAV infection. Unosponized IAV elicited a respiratory burst response in neutrophils which, like that triggered by formylmethionyl-leucyl-phenylalanine (fMLP), involved mediation of signal-transducing GTP-binding proteins and tyrosine kinase activation. The IAV-induced response differed from that provoked by fMLP in that H2O2 was produced without concomitant O2- release. IAV also did not cause extracellular release of granule enzymes in cytochalasin B-treated neutrophils. Using chemiluminescence assays, the respiratory burst response to IAV was found to occur at an intracellular location. These findings may, in part, explain the anomalous nature of the respiratory burst response elicited by IAV and suggest strategies for determining the mechanism of IAV-induced neutrophil deactivation.