Permeability to inhibitors of protein synthesis in virus infected cells

Molecular Biology Reports
|December 1, 1984
PubMed

Insights

Viral infection makes cell membranes permeable to toxins like alpha-sarcin. This cellular permeabilization, observed in various cell lines and viruses, is reversible and sensitive to sulfhydryl reagents.

Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Cell membrane integrity is crucial for cellular function.
  • Viral infections can alter host cell physiology.
  • Selective permeability of the cell membrane restricts entry of large molecules like protein toxins.

Purpose of the Study:

  • To investigate the effect of viral infection on cell membrane permeability.
  • To determine the susceptibility of infected cells to protein toxins.
  • To identify factors influencing virus-induced membrane permeabilization.

Main Methods:

  • Infection of various cell lines (HeLa, KB, BHK-21, L929) with different viruses (EMC, SFV, VSV, Polio).
  • Assessing cell membrane permeabilization using protein toxins, specifically alpha-sarcin.
  • Testing the effect of endocytosis inhibitors, lysosomotropic agents, and sulfhydryl reagents.

Main Results:

  • Viral infection induces cell membrane permeabilization to protein toxins like alpha-sarcin.
  • This phenomenon is observed across multiple cell lines and virus types, dependent on successful viral infection.
  • Permeabilization is not affected by inhibitors of endocytosis or lysosomotropic agents.
  • Cells regain membrane integrity approximately four hours post-infection.
  • Sulfhydryl reagents inhibit the virus-induced cellular permeabilization.

Conclusions:

  • Viral infection can transiently disrupt cell membrane integrity, allowing entry of protein toxins.
  • The mechanism of permeabilization is virus-dependent and distinct from endocytosis.
  • Cellular sulfhydryl groups play a role in maintaining membrane integrity during viral infection.

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