Trever B. Burgon
Graduate Student (Microbiology and Immunology)

B.S. Microbiology, Brigham Young University, 2003.
D325 Fairchild
299 Campus Drive
Stanford CA 94305-5124
Research Summary

Poliovirus infected cells undergo substantial changes in their morphology and metabolism within hours after infection. Host translation is shut off, intracellular membranes are rearranged and protein secretion is inhibited.  Our lab has previously shown that the poliovirus 3A protein can inhibit protein secretion and cause accumulation of secretory cargo in the ER and ER-to-Golgi intermediate compartment. This inhibition decreases the secretion of cytokines and presentation of viral antigens by infected cells.

The goal of my project is understand how and why poliovirus exerts this secretion block. A portion of my work involves the characterization of viral mutations outside of the 3A protein that interfere with the inhibition of secretion. These studies seek to more fully understand the interactions between poliovirus proteins that are involved in this derangement of an infected cell. A second arm of my project uses knockout mice lacking various components of the innate immune system and mutant polioviruses deficient in their ability to inhibit protein secretion to ask why the virus inhibits protein secretion during infection in a mammalian host. My goal is to identify important mediators of immunity that poliovirus attempts to evade by inhibiting protein secretion. In this way, I hope to shed light on the complex relationship between host and pathogen.

Copyright 2006 - 2007. The Laboratory of Karla Kirkegaard, Ph.D. All rights reserved.