Initiation of the respiratory burst of human neutrophils by influenza virus.
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.
D000998:Antiviral Agents; D001790:Blood Physiological Phenomena; D006801:Humans; D066298:In Vitro Techniques; D009980:Influenza A virus; D007251:Influenza, Human / Q000097:blood*; D008163:Luminescent Measurements; D009504:Neutrophils / Q000378:metabolism*; D010101:Oxygen Consumption; D013481:Superoxides / Q000097:blood
D000998:Antiviral Agents; D013481:Superoxides