Journal of NeuroVirology

, Volume 16, Issue 5, pp 405–409

Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replicationin vivo

Authors

  • Steve D Haenchen
    • Department of Molecular BiosciencesUniversity of Kansas
  • Jeff A Utter
    • Department of Molecular BiosciencesUniversity of Kansas
  • Adam M Bayless
    • Department of Molecular BiosciencesUniversity of Kansas
  • Rick T Dobrowsky
    • Department of Pharmacology and ToxicologyUniversity of Kansas School of Pharmacy
    • Department of Molecular BiosciencesUniversity of Kansas
Short communication

DOI: 10.3109/13550284.2010.513030

Cite this article as:
Haenchen, S.D., Utter, J.A., Bayless, A.M. et al. Journal of NeuroVirology (2010) 16: 405. doi:10.3109/13550284.2010.513030

Abstract

Previous studies have shown that herpes simplex virus type 1 (HSV-1) replication is inhibited by the cyclin-dependent kinase (cdk) inhibitor roscovitine. One roscovitine-sensitive cdk that functions in neurons is cdk5, which is activated in part by its binding partner, p35. Because HSV establishes latent infections in sensory neurons, we sought to determine the role p35 plays in HSV-1 replicationin vivo. For these studies, wild-type (wt) and p35-/- mice were infected with HSV-1 using the mouse ocular model of HSV latency and reactivation. The current results indicate that p35 is an important determinant of viral replicationin vivo.

Keywords

cdk5HSV-1HSV-1 latency and reactivationp35p35 knockout mice

Copyright information

© Journal of NeuroVirology, Inc. 2010