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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Human cytomegalovirus regulates bioactive sphingolipids.

Nicholas J Machesky1, Guojuan Zhang, Bindu Raghavan

  • 1Department of Pathology, The Ohio State University, Columbus, Ohio 43210, USA.

The Journal of Biological Chemistry
|July 23, 2008
PubMed
Summary

Human cytomegalovirus (HCMV) infection alters host cell sphingolipid metabolism. This dynamic regulation of sphingolipids impacts virus gene expression and replication.

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Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Sphingolipids are crucial membrane components and signaling molecules in eukaryotic cells.
  • Human cytomegalovirus (HCMV) manipulates host cell signaling for replication.
  • The role of sphingolipid signaling in HCMV infection is largely unknown.

Purpose of the Study:

  • To investigate how HCMV infection affects bioactive sphingolipid levels and their synthesis/degradation enzymes.
  • To determine the impact of these sphingolipid alterations on viral gene expression and replication.

Main Methods:

  • Analysis of sphingolipid accumulation and enzyme activity in HCMV-infected cells.
  • Mass spectrometry-based sphingolipidomic profiling of infected cells.
  • Assessing the effect of de novo sphingolipid synthesis and sphingosine kinase activity on viral processes.

Main Results:

  • HCMV infection increases sphingosine kinase (SphK) activity, leading to elevated sphingosine 1-phosphate (S1P) and dihydrosphingosine 1-phosphate (dhS1P).
  • Increased levels of dhS1P and ceramide at 24 hours post-infection suggest enhanced de novo sphingolipid synthesis.
  • Decreased levels of dihydrosphingosine and dhS1P at 48 hours indicate attenuated de novo synthesis.
  • De novo sphingolipid synthesis and SphK activity were found to directly influence viral gene expression and growth.

Conclusions:

  • HCMV infection dynamically regulates host cell sphingolipid metabolism.
  • These sphingolipid alterations are critical for modulating HCMV gene expression and replication.