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Interactions between human polymorphonuclear leukocytes and influenza virus
Abstract:
The effects of influenza virus A (H3N2) on several functions of human polymorphonuclear leukocytes (PMN) were examined. Incubation of PMN with virus induced chemiluminescence, aggregation, and degranulation of the leukocytes. The amount of chemiluminescence generated increased from 1 X 10(6) to 6 X 10(6) cpm when 2.5 X 10(6) to 2 X 10(7) virus particles were added to 2.5 X 10(6) PMN. Maximal aggregation occurred within 2 min and the response depended on the amount of virus added to the PMN. Release of acid phosphatase by virus-treated PMN was 62 +/- 12% within 1 h compared with 7 +/- 7% by control PMN (P less than 0.005). Incubation of PMN with influenza virus resulted in a diminished phagocytic activity of the phagocytes. PMN from a patient with chronic granulomatous disease were similarly affected. It was thus concluded that the observed defect in phagocytic activity was not due to the reactive oxygen species generated by the PMN during incubation with virus.
Insights
Influenza A (H3N2) virus impairs human polymorphonuclear leukocytes (PMN) function, reducing phagocytosis. This defect is not caused by reactive oxygen species, indicating a direct viral impact on immune cells.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human polymorphonuclear leukocytes (PMN) are critical immune cells.
- Influenza virus A (H3N2) is a significant human respiratory pathogen.
Purpose of the Study:
- To investigate the impact of influenza A (H3N2) on human PMN functions.
- To determine the mechanism behind impaired PMN phagocytosis.
Main Methods:
- Incubation of human PMN with varying concentrations of influenza A (H3N2) virus.
- Measurement of PMN chemiluminescence, aggregation, degranulation, and phagocytic activity.
- Assessment of PMN from a patient with chronic granulomatous disease.
Main Results:
- Influenza A (H3N2) induced PMN chemiluminescence, aggregation, and degranulation.
- Virus-treated PMN showed significantly increased acid phosphatase release.
- Phagocytic activity of PMN was diminished after incubation with the virus.
- PMN from a patient with chronic granulomatous disease exhibited similar defects.
Conclusions:
- Influenza A (H3N2) virus directly affects PMN functions, including degranulation and aggregation.
- A significant defect in PMN phagocytic activity was observed.
- The impaired phagocytosis is not attributable to reactive oxygen species generated by PMN.