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Trypsin increases pseudorabies virus production through activation of the ERK signalling pathway

Béatrice Riteau1, Christiane de Vaureix1, François Lefèvre1

  • 1Unité de Virologie et Immunologie Moléculaires, Institut National de la Recherche Agronomique, Domaine de Vilvert, 78352 Jouy-en-Josas Cedex, France.

The Journal of General Virology
|April 11, 2006
PubMed

Insights

Extracellular proteases, like trypsin, boost herpesvirus replication by activating the ERK 1/2 signaling pathway in infected cells. This suggests proteases play a key role in herpesvirus infections during inflammation.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Extracellular proteases mediate inflammatory processes in viral infections.
  • Proteases like trypsin enhance infectivity for some viruses (e.g., influenza, rotaviruses) via direct proteolytic effects.
  • The role of proteases in modulating herpesvirus replication through cell signaling remains less understood.

Purpose of the Study:

  • To investigate if extracellular proteases modulate the herpesvirus cycle via cell signaling.
  • To determine the effect of trypsin on pseudorabies virus (PRV) production in an in vitro model.
  • To elucidate the signaling pathways involved in protease-mediated viral replication.

Main Methods:

  • Utilized an in vitro model of herpesvirus infection using pseudorabies virus (PRV).
  • Exposed PRV-infected cells to trypsin.
  • Analyzed the activation of the extracellular signal-regulated kinase (ERK) 1/2 signaling pathway.
  • Quantified virus production following trypsin treatment.

Main Results:

  • Exposure of PRV-infected cells to trypsin significantly increased virus production.
  • Trypsin treatment induced synergistic and sustained activation of the ERK 1/2 signaling pathway.
  • ERK 1/2 pathway activation was found to be necessary for the observed increase in viral production.

Conclusions:

  • Herpesviruses may exploit inflammatory contexts and the presence of extracellular proteases to enhance replication.
  • Extracellular proteases, through signaling pathways like ERK 1/2, play a potentially crucial role in herpesvirus infection.
  • These findings highlight a novel mechanism by which viruses interact with the host inflammatory environment.

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