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Effect of influenza virus on phagocytic cells
Abstract:
Many viral infections predispose to bacterial superinfection, and it has been suggested that the increased susceptibility to bacterial infections is at least in part due to the effect of virus on the phagocytic cell function. Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2] ) treated leukocytes with 3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 10(7) EID50 units of influenza virus, PMNs ingested only 35% of the bacteria, whereas control leukocytes ingested over 80%. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.
Insights
Influenza virus impairs neutrophil function, reducing bacterial ingestion and oxidative metabolism. This viral effect on polymorphonuclear leukocytes (PMNs) may be linked to neuraminidase activity, increasing susceptibility to secondary bacterial infections.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Viral infections often lead to bacterial superinfections.
- Impaired phagocytic cell function is a suspected cause of increased bacterial susceptibility during viral infections.
- Mechanisms of viral impact on neutrophil function remain unclear.
Purpose of the Study:
- To investigate the effects of influenza virus on polymorphonuclear leukocyte (PMN) function.
- To elucidate the role of viral neuraminidase in modulating neutrophil activity.
Main Methods:
- Assessing phagocytosis of Staphylococcus bacteria by influenza virus-treated PMNs.
- Measuring oxidative metabolism via chemiluminescence in virus-exposed PMNs stimulated with zymosan.
- Evaluating PMN chemotaxis using an under-agarose assay.
Main Results:
- Influenza virus significantly reduced bacterial ingestion by PMNs (35% vs. >80% in controls).
- Virus exposure markedly suppressed PMN chemiluminescence and reduced cell mobility.
- UV-inactivated virus with intact neuraminidase mimicked these effects, unlike heat-inactivated virus.
Conclusions:
- Influenza virus impairs key neutrophil functions, including phagocytosis, oxidative metabolism, and chemotaxis.
- Viral neuraminidase appears to play a role in mediating these suppressive effects on PMNs.
- These findings suggest a mechanism by which influenza virus increases susceptibility to bacterial superinfections.