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Interactions between human polymorphonuclear leukocytes and influenza virus.

P A Henricks, M E van der Tol, J Verhoef

Scandinavian Journal of Immunology

|December 1, 1985

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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.

Related Experiment Videos

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.