Short communication

Journal of NeuroVirology

, Volume 16, Issue 5, pp 405-409

First online:

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

  • Steve D HaenchenAffiliated withDepartment of Molecular Biosciences, University of Kansas
  • , Jeff A UtterAffiliated withDepartment of Molecular Biosciences, University of Kansas
  • , Adam M BaylessAffiliated withDepartment of Molecular Biosciences, University of Kansas
  • , Rick T DobrowskyAffiliated withDepartment of Pharmacology and Toxicology, University of Kansas School of Pharmacy
  • , David J DavidoAffiliated withDepartment of Molecular Biosciences, University of Kansas Email author 

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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

cdk5 HSV-1 HSV-1 latency and reactivation p35 p35 knockout mice