The influenza virus--infected phagocyte. A model of deactivation.
Influenza A virus has the ability to activate human neutrophils and in turn reduce its subsequent oxidative, chemotactic, and degranulation responses to other stimuli, an effect that may lead to adverse clinical sequelae. Current literature on the mechanism of this effect is reviewed, and preliminary data regarding its biochemical basis presented.
Hartshorn
K L
KL
Boston University School of Medicine, Massachusetts.
Tauber
A I
AI
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002634:Chemotaxis, Leukocyte; D006801:Humans; D009980:Influenza A virus / Q000378:metabolism / Q000502:physiology*; D007251:Influenza, Human / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism; D008264:Macrophages / Q000276:immunology; D008954:Models, Biological; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D010101:Oxygen Consumption; D011014:Pneumonia / Q000209:etiology; D011817:Rabbits; D013481:Superoxides / Q000378:metabolism; D014779:Virus Replication
D007473:Ion Channels; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002118:Calcium