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Plasma membrane cholesterol is required for efficient pseudorabies virus entry

Ann S Desplanques1, Hans J Nauwynck, Dries Vercauteren

  • 1Department of Virology, Parasitology and Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium. Ann.Desplanques@UGent.be

Virology
|May 13, 2008
PubMed

Insights

Cholesterol depletion significantly reduces pseudorabies virus (PRV) entry by stalling viruses at the cell membrane. This suggests cholesterol and lipid rafts are crucial for efficient PRV infection.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Alphaherpesviruses, including human herpes simplex virus and animal pseudorabies virus (PRV), are significant pathogens.
  • Efficient viral entry into host cells is critical for infection.
  • Lipid rafts, cholesterol-rich microdomains in the plasma membrane, are implicated in the entry mechanisms of various viruses.

Purpose of the Study:

  • To investigate the role of cholesterol and lipid rafts in the entry of pseudorabies virus (PRV) into host cells.
  • To determine if cholesterol depletion affects PRV attachment or entry.

Main Methods:

  • Utilizing methyl-beta-cyclodextrin to deplete cholesterol from host cell plasma membranes.
  • Employing fluorescently tagged PRV to visualize and track virus particles.
  • Assessing PRV attachment and entry following cholesterol depletion.
  • Analyzing the localization of PRV virions relative to lipid raft markers like GM1.

Main Results:

  • Depletion of plasma membrane cholesterol significantly reduced PRV entry.
  • Cholesterol depletion did not affect PRV attachment but stalled virus particles at the cell surface.
  • Cholesterol depletion led to the destabilization of lipid raft microdomains.
  • A notable fraction of PRV virions localized near GM1, a lipid raft marker, during the entry process.

Conclusions:

  • Cholesterol is essential for efficient PRV entry into host cells.
  • Cholesterol-rich lipid rafts likely play a critical role in mediating PRV cell entry.
  • Targeting cholesterol or lipid rafts could be a potential strategy to inhibit PRV infection.

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