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Influenza A virus-induced polymorphonuclear leukocyte dysfunction

J S Abramson, D S Lyles, K A Heller

    Infection and Immunity
    |August 1, 1982
    PubMed
    Summary
    This summary is machine-generated.

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    Influenza A virus impairs polymorphonuclear leukocyte (PMN) function. Even brief exposure to the virus causes lasting dysfunction, impacting immune responses to various stimuli.

    Area of Science:

    • Immunology
    • Virology

    Background:

    • Influenza A virus is known to activate polymorphonuclear leukocytes (PMNs).
    • Subsequent stimulation of virus-activated PMNs results in depressed metabolic function, indicating cellular dysfunction.

    Purpose of the Study:

    • To investigate the mechanism by which influenza virus induces PMN dysfunction.
    • To assess the impact of different influenza virus types, exposure times, and secondary stimuli on PMN chemiluminescent activity and function.

    Main Methods:

    • Measuring chemiluminescent activity of PMNs exposed to various influenza A virus strains.
    • Evaluating PMN function after secondary stimulation with phorbol myristate acetate (PMA).
    • Assessing the effect of purified viral glycoproteins in liposomes on PMN chemiluminescence and function.

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    Main Results:

    • Different intact influenza virus types induced varying chemiluminescent activities.
    • All tested viruses caused equivalent depression of PMN response upon subsequent PMA stimulation.
    • Purified viral glycoproteins did not induce PMN dysfunction.
    • Depressed PMN function was observed after only 5 minutes of virus incubation.
    • Dysfunction affected both receptor-dependent and -independent stimuli.

    Conclusions:

    • Influenza A virus directly induces PMN dysfunction, independent of initial activation levels.
    • The mechanism of dysfunction appears to involve the intact virus particle, not just surface glycoproteins.
    • Rapid and sustained impairment of PMN function by influenza virus has significant implications for host immunity.