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Vesicular stomatitis virus induced membrane changes: a spin label study.

P L Gutierrez, L H Davis, R Pottathil

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    |August 13, 1984
    PubMed
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    Vesicular Stomatitis Virus (VSV) entry increases cell membrane rigidity. Interferon alpha did not prevent this VSV-induced change, despite offering antiviral protection.

    Area of Science:

    • Virology
    • Cell Biology
    • Biophysics

    Background:

    • Vesicular Stomatitis Virus (VSV) is a model virus for studying viral entry mechanisms.
    • Cell membrane properties play a crucial role in viral infection processes.
    • Interferon alpha is a key component of the innate immune system with known antiviral effects.

    Purpose of the Study:

    • To investigate the impact of synchronized VSV entry on the biophysical properties of human cell membranes.
    • To determine if interferon alpha treatment affects cell membrane fluidity or mitigates VSV-induced membrane alterations.

    Main Methods:

    • Cultured human cells were labeled with spin probes for Electron Spin Resonance Spectroscopy.
    • Synchronized entry of VSV into these labeled cells was induced.

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  • Membrane rigidity changes were measured using Electron Spin Resonance Spectroscopy.
  • The effect of homologous interferon alpha on membrane fluidity and VSV-induced changes was assessed.

    • Main Results:

    • Synchronized VSV entry led to a significant increase in the rigidity of cell membranes.
    • Interferon alpha treatment did not alter basal membrane fluidity.
    • Interferon alpha did not significantly inhibit the increase in membrane rigidity caused by VSV entry.

    Conclusions:

    • VSV entry induces biophysical changes in host cell membranes, specifically increasing rigidity.
    • Interferon alpha's antiviral mechanism may not involve direct modulation of membrane fluidity or prevention of VSV-induced rigidity changes.