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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

Human cytomegalovirus infection inhibits epidermal growth factor (EGF) signalling by targeting EGF receptors

J A Fairley1, J Baillie2, M Bain2

  • 1Division of Biochemistry and Molecular Biology, University of Glasgow, Glasgow, UK2.

The Journal of General Virology
|October 22, 2002
PubMed

Insights

Human cytomegalovirus (HCMV) infection disrupts epidermal growth factor receptor (EGFR) function, decreasing its cell-surface expression and inhibiting EGF signaling. This suggests HCMV isolates cells from external signals to optimize virus production.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Human cytomegalovirus (HCMV) is a ubiquitous virus that establishes lifelong infections.
  • HCMV infection perturbs cellular functions, including cell cycle control, transcription, and immunoregulation.
  • HCMV manipulates host cells to favor viral persistence and replication.

Purpose of the Study:

  • To investigate the effect of HCMV infection on external cellular signaling pathways.
  • To determine if HCMV disrupts the function of the epidermal growth factor receptor (EGFR).

Main Methods:

  • Assessing cell-surface EGFR expression post-HCMV infection.
  • Measuring steady-state levels of EGFR protein.
  • Evaluating EGF-mediated EGFR autophosphorylation.
  • Utilizing a mutant HCMV lacking known MHC Class I down-regulation factors.

Main Results:

  • HCMV infection significantly decreased cell-surface EGFR expression.
  • A corresponding reduction in EGFR protein levels was observed.
  • HCMV inhibited EGFR autophosphorylation in response to EGF stimulation.
  • EGFR down-regulation occurred independently of known viral mechanisms for MHC Class I modulation, indicating a novel viral function.

Conclusions:

  • HCMV infection disrupts EGFR signaling, a key pathway for external cellular communication.
  • This disruption is mediated by a previously unrecognized viral mechanism.
  • HCMV appears to 'isolate' infected cells from host signals, promoting a virus-centric environment for replication.

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