Grant: Project Grant

We study the herpes simplex viruses HSV-1 and HSV-2, which infect ~3.7 billion and ~500 million people, respectively. These viruses cause lifelong infections for which there is no cure. Resistance to existing HSV drugs is a problem, particularly in people with weakened or underdeveloped immune systems who often suffer from the most serious forms of HSV disease. A deeper understanding of how these viruses assemble new copies of themselves within an infected cell is required to identify antiviral drugs targeted towards disrupting viral assembly. We are studying a protein made by HSV, pUL16, that is critical for several steps in viral assembly. Our preliminary experiments have identified several human proteins that appear to interact with pUL16. We hypothesize that these human proteins work together with pUL16 to facilitate the assembly of new virus particles. The work described in this proposal seeks to determine how pUL16 interacts with human proteins and the significance of these interactions for viral assembly. A long-term goal of this research is to use the insight we gain on the interactions between pUL16 and human proteins to devise ways to disrupt these interactions and thus disrupt viral assembly. Disrupting viral assembly within a cell will prevent viral spread within the infected individual and, ultimately, between an infected individual and uninfected people within a population.