Depression of Human Neutrophil Motility by Influenza Virus In Vitro

Abstract

After in vitro treatment of human peripheral neutrophils for 60 min at 37°C with purified influenza A virus, their random locomotion (no chemoattractant), chemokinesis (migration in the presence of a chemoattractant without a gradient), and chemotaxis were depressed, as determined by a modification of the Boyden method. The inhibition was accentuated by the presence of human serum devoid of antibodies to the virus. A strain of influenza B virus did not depress neutrophil motility at the same concentration and agglutinated the neutrophils at higher concentrations. Antiserum treatment partly abolished the inhibitory activity of the influenza virus. Inactivation of the virus infectivity with Tween 80 and ether did not change the ability of the virus to inhibit neutrophil motility. Bacterial neuraminidase did not inhibit neutrophil motility. Pretreatment of neutrophils with amantadine hydrochloride, which has been reported to block viral replication in its early stages, did not modify the depression of neutrophil motility by influenza A virus. The results give additional support to the suggested mechanism of depressed neutrophil function as a cause of bacterial superinfection after influenza.