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

• Published in: Journal of neurovirology Vol. 16; no. 5; pp. 405 - 409
• Main Authors: Haenchen, Steve D, Utter, Jeff A, Bayless, Adam M, Dobrowsky, Rick T, Davido, David J
• Format: Journal Article
• Language: English
• Published: Heidelberg Journal of Neurovirology 01.10.2010; Springer
• Subjects: Animals; Biological and medical sciences; Herpes Simplex - virology; Herpesvirus 1, Human - physiology; Host-Pathogen Interactions; Human viral diseases; Infectious diseases; Medical sciences; Mice; Mice, Inbred C57BL; Mice, Knockout; Nerve Tissue Proteins - physiology; Viral diseases; Viral diseases of the nervous system; Viral diseases with cutaneous or mucosal lesions and viral diseases of the eye; Virus Activation; Virus Latency; HSV-1 latency and reactivation; Nervous system diseases; Reactivation; cdk5; Herpesviridae; Alphaherpesvirinae; Rodentia; Protein; Infection; Virus; Vertebrata; HSV-1; Mammalia; p35; Mouse; Animal; Viral disease; Human herpesvirus 1; Replication; p35 knockout mice
• ISSN: 1355-0284; 1538-2443
• DOI: 10.3109/13550284.2010.513030

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 replication in 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 replication in vivo.