Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replicationin vivo
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.
Keywordscdk5 HSV-1 HSV-1 latency and reactivation p35 p35 knockout mice
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- Fields BN, Knipe DM, Howley PM (2007).Fields Virology, 5th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.Google Scholar
- National Research Council (1996).Guide for the care and use of laboratory animals. Washington, DC: National Academy Press.Google Scholar
- Ohshima T, Ward JM, Huh CG, Longenecker G, Veeranna, Pant HC, Brady RO, Martin LJ, Kulkarni AB (1996). Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death.Proc Natl Acad Sci U S A 93: 11173–11178.PubMedCrossRefGoogle Scholar