Influenza A virus enhances the human polymorphonuclear leukocyte chemoluminescence response without effecting inhibition by trifluoperazine.

Influenza A virus has been demonstrated to enhance superoxide generation and chemoluminescence (CL) in human polymorphonuclear leucoytes (PMNs) under in vitro conditions. Although the mechanisms of virus-enhanced neutrophil activity is not established, calmodulin concentrations are known to increase in some virus-transformed cells. In the following experiments, we evaluated the PMN response to the calmodulin-inhibitor trifluoperazine (TFP) after an incubation with influenza A virus. Human PMNs were isolated from whole blood and were incubated with either influenza A virus (at 50% egg-infective dose per 1 leukocyte) or noninfected allantoic fluid. After incubation with influenza virus, the CL response of isolated PMNs to opsonized zymosan particles was measured. The influenza virus-treated PMNs had a mean (+/- SEM, n = 16) increase in light emission of 59.5 +/- 7.7%. TFP, in concentrations of 6 micron, 8 micron, and 10 microM, inhibition of CL was similar in influenza virus and allantoic fluid-treated neutrophils. These data suggest that, although the influenza A virus enhanced the PMN "respiratory burst" to opsonized zymosan particles, it did not alter the cell response to one calmodulin inhibitor, TFP.