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Forced degradation of Fas inhibits apoptosis in adenovirus-infected cells

A E Tollefson1, T W Hermiston, D L Lichtenstein

  • 1Department of Molecular Microbiology and Immunology, St Louis University School of Medicine, Missouri 63104-1004, USA.

Nature
|May 16, 1998
PubMed

Insights

Adenovirus RID protein complex prevents cell death by internalizing and degrading the Fas receptor. This mechanism helps infected cells evade apoptosis and promotes viral survival.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • DNA viruses employ mechanisms to evade host antiviral defenses.
  • Tumor Necrosis Factor (TNF)-induced apoptosis is a key antiviral defense.
  • Adenoviruses encode proteins that inhibit apoptosis during infection.

Purpose of the Study:

  • To investigate the mechanism by which adenovirus inhibits Fas-mediated apoptosis.
  • To determine the role of the adenovirus RID (receptor internalization and degradation) protein complex in this process.

Main Methods:

  • Investigated the interaction of adenovirus RID complex with cell-surface receptors.
  • Utilized techniques to track receptor internalization and degradation pathways.
  • Examined the effect of RID on Fas receptor localization and stability.

Main Results:

  • Adenovirus RID complex mediates the internalization of cell-surface Fas receptor.
  • Fas receptor is subsequently degraded within lysosomes following internalization by RID.
  • RID also internalizes the epidermal growth factor receptor but not transferrin receptor or MHC class I antigens.

Conclusions:

  • Adenovirus RID complex actively removes Fas from the cell surface, preventing Fas-mediated apoptosis.
  • This evasion strategy enhances infected cell survival, promoting viral propagation.
  • Fas receptor internalization and degradation by viral proteins is a novel mechanism of immune evasion.

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