Grant: Operating Grant

Many viruses alter host cell functions to promote virus replication and evade host antiviral responses, for example by activating the PI3-kinase/Akt pathway to enhance cell survival and translation of viral mRNAs while inhibiting pathways that detect and control pathogens. We and our collaborators have discovered that the herpes simplex virus protein VP11/12 plays key roles in modulating host signaling: it is essential for virus-induced activation of Akt, and it is also able to disarm signaling through the T cell receptor, thereby dampening antiviral immunity. This research project focuses on determining exactly how VP11/12 achieves these remarkable effects, and delineating their impact on virus replication. The results will increase our understanding of viral replication strategies, and perhaps point to new approaches to controlling virus infection.