Suppression of endocytosis in neutrophils by influenza A virus in vitro.
The effect of influenza A virus on the endocytic pathway in polymorphonuclear leukocytes (PMNLs) and the relationship of altered endocytic activity to virus-induced inhibition of other PMNL functions were examined with virus that caused decreased phagosomelysosome fusion and bacterial killing (depressing virus [DV]) and virus that did not (non-DV). Binding of both viruses to PMNL surface receptors was similar, but uptake of DV into PMNLs was decreased compared with that of non-DV. Both viruses were associated with the PMNL plasma membrane and were in endosomes. DV caused less stimulation of pinocytosis than did non-DV. The rate of exocytosis of fluoresceinated-dextran (FL-dextran) from cells stimulated with DV was significantly less than for non-DV. When PMNLs were pretreated with buffer, DV, or non-DV and then exposed to FL-dextran and N-formylmethionylleucylphenylalanine, the pinocytosis of FL-dextran was significantly less in cells pretreated with DV as compared with non-DV or buffer.
D004705:Endocytosis; D006801:Humans; D066298:In Vitro Techniques; D009980:Influenza A virus / Q000648:ultrastructure; D007251:Influenza, Human / Q000276:immunology*; D008854:Microscopy, Electron; D009504:Neutrophils / Q000382:microbiology* / Q000502:physiology / Q000648:ultrastructure; D010873:Pinocytosis; D013347:Subcellular Fractions / Q000382:microbiology