“Coming from a small private liberal arts college background, I really liked that Wake Forest's Department of Microbiology and Immunology was small and close-knit. I'd always felt that smaller schools, which can provide a great deal of student-professor interaction, paired with rigorous academics is an unbeatable combination and that is just the kind of environment that Wake Forest offers.”

Research

Adenovirus both triggers the cellular DNA damage response pathway and employs methods by which to suppress the host response. The E1B-55K-/E4orf3- double mutant virus is defective in suppressing the DNA damage response and has been observed to mediate an increase in rates of cell death in many cell lines. One of the ways in which the double mutant virus is defective is its inability to antagonize the DNA-damage response protein NBS1 through the adenoviral protein E4orf3. This E4orf3-dependent deficiency in suppressing the DNA damage response pathway is hypothesized to result in increased rates of cell death. Early stage bladder cancer cells have been seen to have an intrinsically active DNA damage response pathway, leading to the hypothesis that these cells may be more susceptible to cell killing by the E1B-55K-/E4orf3- double mutant virus.

My research seeks to identify the mechanisms of cell death that occur in response to E1B-55K/E4orf3 double-mutant virus infection, elucidate the role of E4orf3 in delaying cell death in wild-type and E1B-55K- single mutant virus infections, and determine the relationship between the level of activation of the host DNA-damage response activation levels and virus-mediated cell killing.