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Growth characteristics of influenza virus concerning the binding of virus by host cells

W W ACKERMANN, N ISHIDA, H F MAASSAB

    The Journal of Experimental Medicine
    |November 1, 1955
    PubMed

    Insights

    Influenza virus binds to membranes, retaining infectivity but not initiating replication. This reversible binding involves two distinct mechanisms sensitive to RDE and AMPS, suggesting an abortive infection process.

    Area of Science:

    • Virology
    • Cell Biology
    • Biochemistry

    Background:

    • Influenza virus interaction with host cells is crucial for infection.
    • Understanding viral binding mechanisms is key to developing antiviral strategies.

    Purpose of the Study:

    • To investigate the binding characteristics of influenza virus to chorioallantoic membranes.
    • To elucidate the nature of viral binding and its effect on viral infectivity and replication.

    Main Methods:

    • Incubation of influenza virus with chorioallantoic membranes.
    • Washing experiments to assess binding reversibility.
    • Treatment of membranes with Receptor Destroying Enzyme (RDE) and Alpha-2-macroglobulin (AMPS) to study binding modulation.

    Main Results:

    • Influenza virus binds to chorioallantoic membranes, retaining infectious properties but not initiating viral replication.
    • Binding is partially reversible, suggesting an equilibrium-type interaction.
    • Receptor Destroying Enzyme (RDE) and Alpha-2-macroglobulin (AMPS) modulate binding, with combined treatment preventing stable binding.
    • Bound virus, even when initiating activity is present, cannot promote viral increase.

    Conclusions:

    • Influenza virus binding to host cell receptors is complex, involving at least two distinct, site-specific binding mechanisms.
    • One binding type is sensitive to Receptor Destroying Enzyme (RDE), while the other is blocked by Alpha-2-macroglobulin (AMPS).
    • The binding of infectious virus appears to be an abortive attempt at initiating infection, offering insights into viral entry and early replication stages.
    Keywords:
    INFLUENZA VIRUSES

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