David Davido

Associate Professor
Primary office:
(785) 864-4022
7047 Haworth


Molecular virology and pathogenesis of herpes simplex virus.

Herpes simplex virus type 1 (HSV-1) is a common and significant human pathogen which 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 or virions, but the presence of the viral DNA in the latently infected neurons. Importantly, latent HSV-1 can be reactivated to produce infectious virus by a variety of ill-defined stimuli such as stress or emotional or physical trauma.

Infected cell protein 0 (ICP0) is one of the first HSV-1 proteins to be expressed upon infection of cells in culture and is a potent and promiscous transactivator of HSV-1 gene expression. Though ICP0 is not required for viral replication, it confers a significant growth advantage on the virus in non-dividing cells and in vivo, and during reactivation from latency. In addition, ICP0 localizes to and subsequently disrupts nuclear structures known as nuclear domain 10 (ND10) which are thought to be important for regulating cellular differentiation, proliferation, and antiviral responses. ICP0’s ND10 disrupting activity has been linked to its transactivating activity. Collectively, these observations indicate that ICP0 is a key determinant in the switch between productive and latent infections of HSV-1.

My research interests are to understand the interactions between viral and cellular factors that regulate the HSV-1 lifecycle, relating findings from our studies to recurrent herpetic disease. For this purpose, my research has focused on the interaction between ICP0 and cellular factors. Specifically, it has been previously demonstrated that phosphorylation regulates the activities of many viral and cellular proteins. My laboratory is interested in determining whether the phosphorylation of ICP0 alters its function. Using variety of biophysical, biochemical, and genetic approaches, we have identified several regions of phosphorylation on ICP0 and determined that mutation of these regions alter selected activities of ICP0 including its transactivating activity. Mutant forms of ICP0 with mutations in individual phosphorylation sites in these regions are being tested currently to identify specific phosphorylation sites critical for ICP0 function. From these studies, it will be possible to determine which sites and the potential cellular and viral kinases that phosphorylate these sites modulates the function of ICP0 which, in turn, regulates the lifecycle of HSV-1.

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