Characterization of the chemotactic defect in polymorphonuclear leukocytes exposed to influenza virus in vitro.
The mechanism by which influenza virus interferes with polymorphonuclear leukocyte (PMN) chemotaxis was investigated. Incubation of human PMN with influenza A virus in vitro for 30 minutes significantly decreased PMN migration under agarose in response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) or zymosan-activated serum. Virus-treated PMN tended to aggregate in the under-agarose assay. Aggregation was avoided by using a more dilute PMN suspension in filter assays. Virus treatment significantly decreased migration through 100-micron thick cellulose nitrate filters but had no effect on migration through 10-micron thick polycarbonate filters or on PMN bipolar shape change. Virus was not chemotactic in the polycarbonate filter assay and did not induce shape change in purified PMN. It was concluded that influenza virus did not interfere with the ability of PMN to recognize a chemoattractant, undergo shape change, and move a short distance but did limit the extent of migration. Inhibition could not be explained by chemotactic deactivation, since the virus was not chemotactic.
D000914:Antibodies, Viral / Q000032:analysis; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte; D003101:Collodion; D005374:Filtration; D006801:Humans; D009980:Influenza A virus / Q000276:immunology / Q000502:physiology*; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology*; D011076:Polycarboxylate Cement; D012685:Sepharose
D000914:Antibodies, Viral; D011076:Polycarboxylate Cement; C005506:polycarbonate; D003101:Collodion; D012685:Sepharose