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

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.

• Authors: Heba H Mostafa, Jessica M van Loben Sels, David J Davido
• Journal: Journal of virology (J Virol) Vol. 89 Issue 9 Pg. 5171-5 (May 2015) ISSN: 1098-5514 [Electronic] United States
• PMID: 25694605 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015, American Society for Microbiology. All Rights Reserved.

Chemical References

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

Topics

• 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