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Pseudorabies virus US3 protein kinase mediates actin stress fiber breakdown

Geert Van Minnebruggen1, Herman W Favoreel, Liesbeth Jacobs

  • 1Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, 9820 Merelbeke, Belgium.

Journal of Virology
|July 30, 2003
PubMed

Insights

Pseudorabies virus (PRV) infection disrupts host cell actin stress fibers. The viral US3 serine/threonine protein kinase is key to this disruption, even when US3 acts alone.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Viral infections can disrupt host cytoskeleton, aiding viral replication.
  • Pseudorabies virus (PRV), a swine alphaherpesvirus, previously shown to induce actin stress fiber breakdown in swine kidney cells.

Purpose of the Study:

  • To identify the specific viral component responsible for PRV-induced actin stress fiber breakdown.
  • To investigate the role of the US3 protein kinase in cytoskeletal disruption.

Main Methods:

  • Utilized PRV deletion mutants to analyze viral protein functions.
  • Employed transfection assays to study the US3 protein kinase independently.
  • Examined actin stress fiber integrity in infected and transfected cells.

Main Results:

  • The US3 serine/threonine (S/T) protein kinase was identified as the viral factor responsible for actin stress fiber breakdown.
  • PRV US3 alone, when sufficiently localized in the nucleus, can induce actin stress fiber breakdown.
  • This effect was observed across different cell lines infected with PRV.

Conclusions:

  • The PRV US3 protein kinase is a critical determinant of viral-induced actin cytoskeletal disruption.
  • US3 kinase activity is sufficient to cause actin stress fiber breakdown, highlighting its significant role in viral pathogenesis.

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