Phosphorylation state of the cap-binding protein eIF4E during viral infection

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Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
08:47

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

M Kleijn1, C L Vrins, H O Voorma

  • 1Department of Molecular Cell Biology, University of Utrecht, The Netherlands.

Virology
|March 15, 1996
PubMed

Insights

Viral infection dephosphorylates eukaryotic translation initiation factor 4E (eIF4E), a key protein in host shut-off. Encephalomyocarditis virus (EMCV) entry and decreased cap-dependent translation trigger this essential process.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Eukaryotic translation initiation factor 4E (eIF4E), the cap-binding protein, is crucial for host cell control during viral infections.
  • Adenovirus and influenza virus infections are known to cause eIF4E dephosphorylation, suggesting viral involvement.

Purpose of the Study:

  • To investigate the ability of various viruses to alter eIF4E phosphorylation.
  • To elucidate the mechanism behind viral-induced eIF4E dephosphorylation.

Main Methods:

  • Infection of cells with encephalomyocarditis virus (EMCV), poliovirus, Semliki Forest virus, and reovirus.
  • Treatment with phosphatase inhibitor okadaic acid to manipulate eIF4E phosphorylation levels.
  • Infection with UV-inactivated EMCV to distinguish between viral entry and replication effects.
  • Use of protein synthesis inhibitors (pactamycin and cycloheximide).

Main Results:

  • EMCV and poliovirus infections led to eIF4E dephosphorylation, unlike Semliki Forest virus and reovirus.
  • Artificial enhancement of eIF4E phosphorylation did not alter EMCV or poliovirus infection kinetics or host shut-off.
  • UV-inactivated EMCV demonstrated that virus binding or entry initiates eIF4E dephosphorylation.
  • Blocking protein synthesis also induced eIF4E dephosphorylation.

Conclusions:

  • Encephalomyocarditis virus (EMCV) entry into cells triggers eIF4E dephosphorylation.
  • Decreased cap-dependent translation enhances the effect of EMCV entry on eIF4E dephosphorylation.
  • eIF4E dephosphorylation is a significant mechanism in viral host shut-off.

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