Herpes simplex virus 1 upregulates p35, alters CDK-5 localization, and stimulates CDK-5 kinase activity during acute infection in neurons

J Virol. 2015 May;89(9):5171-5. doi: 10.1128/JVI.00106-15. Epub 2015 Feb 18.

Abstract

The cyclin-dependent kinase 5 (CDK-5) activating protein, p35, is important for acute herpes simplex virus 1 (HSV-1) replication in mice. This report shows that HSV-1 increases p35 levels, changes the primary localization of CDK-5 from the nucleus to the cytoplasm, and enhances CDK-5 activity during lytic or acute infection. Infected neurons also stained positive for the DNA damage response (DDR) marker γH2AX. We propose that CDK-5 is activated by the DDR to protect infected neurons from apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cyclin-Dependent Kinase 5 / metabolism*
  • DNA Damage
  • Herpesvirus 1, Human / physiology*
  • Histones / analysis
  • Host-Pathogen Interactions*
  • Mice, Knockout
  • Neurons / virology*
  • Phosphotransferases / biosynthesis*
  • Virus Replication*

Substances

  • Cdk5r1 protein, mouse
  • Histones
  • gamma-H2AX protein, mouse
  • Phosphotransferases
  • Cyclin-Dependent Kinase 5
  • Cdk5 protein, mouse