Herpes Simplex Virus ICP0 Phosphorylation Site Mutant

University of Kansas
posted on 08/07/2009

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Description: Herpes simplex virus type 1 (HSV-1) is a common and significant human pathogen that causes a variety of diseases, ranging from cold sores and potentially blinding ocular infections to life-threatening encephalitis. HSV-1 establishes lifelong latent infections in neuronal cells, which reactivate periodically. Its lifecycle can be described in two specific stages of infection: productive and latent. Productive infection is characterized by the expression of nearly all (~100) viral genes in epithelial cells and fibroblasts at the periphery and the sensory neurons that innervate the site infection. Latent infection is defined as a lack of infectious virus. Infected cell protein 0 (ICP0) is a nuclear phosphoprotein and is one of the first HSV-1 proteins to be expressed upon infection of cells in culture. ICP0 is a key determinant in the switch between productive and latent infections of HSV-1. It has been previously demonstrated that phosphorylation regulates the activities of many viral proteins. KU researchers sought to determine the role of ICP0 phosphorylation in HSV-1 replication. As an initial goal towards this aim, they identified at least one region of phosphorylation in ICP0 and mutated phosphorylation sites in this region, introducing them into the HSV-1 genome. Upon testing this viral mutant of ICP0 in vivo, the data indicates that alteration of ICP0's phosphorylation state significantly impairs HSV-1 replication compared to wild-type HSV-1. Applications: Vaccine and Anti-HSV therapeutics Patent: Pending Confidential Disclosure Agreement (CDA): KU is willing to enter into a CDA for the purpose of negotiating a License Agreement. If you are interested in learning details of this invention, please contact: Aswini K. Betha, Ph.D. (abetha@ku.edu Ph: 913-588-5713)