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. 1981 Jun;32(3):1200–1205. doi: 10.1128/iai.32.3.1200-1205.1981

Initiation of the respiratory burst of human neutrophils by influenza virus.

E L Mills, Y Debets-Ossenkopp, H A Verbrugh, J Verhoef
PMCID: PMC351579  PMID: 6265373

Abstract

The role of the oxygen-dependent microbicidal systems of polymorphonuclear neutrophils in virus inactivation is not known. We found that isolated neutrophils responded to incubation with purified influenza virus A particles by consumption of oxygen, generation of chemiluminescence, and production of superoxide; these reactions occurred in the absence of serum. Resting leukocyte oxygen consumption doubled in the presence of virus; the average rate of consumption 2 to 12 min after virus was added was 1.54 nmol/10(7) cells per min. Live virus also stimulated superoxide production in a dose-dependent manner at a rate up to 4.54 nmol/10(7) cells per min. Luminol-amplified chemiluminescence was a rapid dose-dependent reaction which peaked 2 to 4 min after live or ultraviolet light-inactivated virus was added. No light was emitted when heat-inactivated virus particles were used, suggesting that heat-labile factors on the virus envelope may be involved in oxidative stimulation. Virus-stimulated neutrophils from a patient with chronic granulomatous disease emitted no light. The evidence that virus initiated the respiratory burst of neutrophils provided a potential mechanism for virus destruction, either by direct intracellular inactivation or by neutrophil-mediated cellular cytotoxicity of virus-infected target cells.

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Selected References

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