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Membrane changes during viral infection.

C A Pasternak, M A Gray, K J Micklem

    Bioscience Reports
    |August 1, 1982
    PubMed
    Summary
    This summary is machine-generated.

    Viruses affect cell membranes differently during entry and exit. Not all viruses cause membrane leakage, and generalized leakiness is not required for virus release, challenging previous hypotheses.

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    Area of Science:

    • Virology
    • Cell Biology
    • Membrane Biophysics

    Background:

    • Viruses interact with host cell membranes during their life cycle.
    • Previous hypotheses suggested generalized membrane leakiness might be necessary for viral replication and release.

    Purpose of the Study:

    • To investigate the effects of viral entry and exit on the surface membrane of susceptible host cells.
    • To determine if viral activity causes non-specific membrane permeability changes.
    • To test the hypothesis that generalized membrane leakiness is a prerequisite for virus synthesis and release.

    Main Methods:

    • Studied the surface membrane function of cells infected with various viruses.
    • Monitored for changes in membrane permeability to low-molecular-weight compounds.

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  • Assessed nutrient uptake and membrane potential during viral exit.

    • Main Results:

    • Haemolytic paramyxoviruses induced non-specific leakage of low-molecular-weight compounds during entry.
    • Other viruses did not exhibit this non-specific leakage effect during entry.
    • Viral exit did not consistently cause membrane changes; some viruses showed no effect, while others altered nutrient uptake and decreased membrane potential.

    Conclusions:

    • Viral effects on cell surface membranes vary significantly depending on the virus and the stage of the viral life cycle (entry vs. exit).
    • The observed membrane alterations do not support the hypothesis that generalized membrane leakiness is a prerequisite for virus particle synthesis and release.
    • Specific viral mechanisms, rather than general membrane disruption, likely govern virus-cell interactions.