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Varicella zoster virus glycoprotein gpI is selectively phosphorylated by a virus-induced protein kinase

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Varicella zoster virus glycoprotein I (VZV gpI) is selectively phosphorylated in infected cells. A virus-induced protein kinase found in infected cells targets VZV gpI for this modification.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biochemistry

Background:

  • Varicella zoster virus (VZV) is a human herpesvirus responsible for chickenpox and shingles.
  • VZV encodes several glycoproteins essential for viral infectivity and host cell interaction.
  • Post-translational modifications of viral proteins can significantly impact viral pathogenesis.

Purpose of the Study:

  • To investigate the post-translational modification of Varicella zoster virus glycoprotein I (VZV gpI).
  • To identify the mechanism and selectivity of VZV gpI phosphorylation.
  • To characterize the enzyme responsible for VZV gpI phosphorylation.

Main Methods:

  • Analysis of VZV-infected human cell monolayers.
  • In vitro kinase assays using [gamma-32P]ATP and purified VZV glycoproteins.
  • Phosphoamino acid analysis and enzymatic treatment of phosphorylated VZV gpI.

Main Results:

  • Varicella zoster virus glycoprotein I (VZV gpI) undergoes selective phosphorylation in infected cells, unlike VZV gpII and gpIII.
  • Phosphorylation occurs on serine and threonine residues of the polypeptide backbone and is not inhibited by glycosylation inhibitors.
  • A novel virus-induced protein kinase (Mr 50,000) present in infected cells specifically phosphorylates VZV gpI in vitro and is located on the plasma membrane.

Conclusions:

  • VZV gpI is selectively phosphorylated via a virus-induced protein kinase.
  • This phosphorylation event is a distinct post-translational modification occurring on the polypeptide backbone.
  • The virus-induced protein kinase may play a role in VZV replication or pathogenesis.

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