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Herpes Simplex Virus 1 US3 Phosphorylates Cellular KIF3A To Downregulate CD1d Expression.

Ran Xiong1, Ping Rao1, Seil Kim1

  • 1Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.

Journal of Virology
|April 17, 2015
PubMed
Summary

Herpes simplex virus 1 (HSV-1) uses its US3 protein kinase to phosphorylate KIF3A, a motor protein. This action downregulates CD1d expression, aiding HSV-1 immune evasion and NKT cell suppression.

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Herpes simplex virus 1 (HSV-1) is a common human pathogen causing significant infections.
  • HSV-1 evades the host immune system, particularly innate immunity, through mechanisms not fully understood.
  • Previous work showed HSV-1 downregulates CD1d and suppresses NKT cells via its US3 protein kinase.

Purpose of the Study:

  • To identify the cellular targets of HSV-1 US3 protein kinase.
  • To elucidate the mechanism by which US3 suppresses CD1d cell surface expression.
  • To understand how HSV-1 evades NKT cell-mediated immunity.

Main Methods:

  • Investigated cellular substrates phosphorylated by US3.
  • Utilized in vitro and in infected cell assays to study KIF3A phosphorylation by US3.
  • Employed mass spectrometry to identify phosphorylation sites on KIF3A.
  • Assessed the impact of KIF3A phosphorylation ablation on CD1d expression.

Main Results:

  • Identified KIF3A, a type II kinesin motor protein, as critical for CD1d cell surface expression.
  • Demonstrated that HSV-1 US3 phosphorylates KIF3A both in vitro and in infected cells.
  • Determined that serine 687 is the primary phosphorylation site on KIF3A by US3.
  • Showed that disrupting KIF3A phosphorylation prevents US3-mediated CD1d downregulation.

Conclusions:

  • HSV-1 US3 protein kinase phosphorylates KIF3A at serine 687.
  • This phosphorylation event is the key mechanism for US3-mediated suppression of CD1d cell surface expression.
  • Understanding this viral immune evasion strategy can inform future vaccine development for herpesviruses.