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Inhibition of protein kinases C prevents murine cytomegalovirus replication

Natalia Kučić1, Hana Mahmutefendić1, Pero Lučin1

  • 1Department of Physiology and Immunology, Medical Faculty, University of Rijeka, Braće Branchetta 20, 51000 Rijeka, Croatia.

The Journal of General Virology
|July 22, 2005
PubMed

Insights

Murine cytomegalovirus (MCMV) infection relies on protein phosphorylation. Protein kinase C (PKC) activity is essential for early MCMV replication, specifically diacylglycerol/phorbol ester-dependent, calcium-independent pathways.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Murine cytomegalovirus (MCMV) infection requires host cell machinery for its early replication steps.
  • Cellular regulatory mechanisms, particularly protein phosphorylation, are critical for MCMV's initial infection stages.
  • Protein kinases C (PKCs) are implicated in various cellular processes, including viral infections.

Purpose of the Study:

  • To investigate the role of protein phosphorylation mediated by protein kinases C (PKCs) in the early events of MCMV infection.
  • To identify specific PKC subclasses involved in the establishment of MCMV infection.

Main Methods:

  • Utilized protein kinase inhibitors (H-7, sangivamycin, calphostin C, bisindolylmaleimide II) and Ca(2+)/calmodulin inhibitors (EDTA, W7).
  • Assessed inhibitory effects on MCMV replication by measuring IE1 and E1 protein expression via immunofluorescence and Western blot.
  • Quantified the production of infectious virions in cell culture to determine replication efficiency.

Main Results:

  • The broad-spectrum kinase inhibitor H-7 blocked MCMV replication in a dose-dependent and reversible manner, indicating an early-stage block.
  • Specific PKC inhibitors, Ca(2+)/calmodulin inhibitors, and phorbol esters were used to dissect the contribution of different PKC subclasses.
  • Results pinpointed diacylglycerol/phorbol ester-dependent but calcium-independent PKCs as essential for MCMV infection establishment.

Conclusions:

  • Protein kinase C activity is crucial for the early stages of MCMV infection.
  • Diacylglycerol/phorbol ester-dependent, calcium-independent PKC pathways are vital for MCMV entry and replication initiation.
  • Targeting these specific PKC pathways could offer strategies to inhibit MCMV infection.

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