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B.S., University of Oregon, Eugene, OR, 2008
M.S., George Washington University, Washington, DC, 2013
Honors and awards:
Mycobacterium tuberculosis (Mtb), the most common causative agent of tuberculosis (TB) persists in 90% of infected individuals by establishing a latent infection. The bacillus primarily survives and replicates in the phagosomes of resident macrophages in a host’s lungs. A critical immune response to control Mtb is the activation of these macrophages by the inflammatory cytokine interferon-gamma (IFN-γ), which stimulates antimicrobial functions such as reactive oxygen and nitrogen species, maturation and acidification of phagosomes. However, Mtb has devised several counter-immune mechanisms in order to evade the host’s robust immune responses and remain in a latent and persistent state. Latent bacteria can become reactivated if left untreated, resulting in an active TB infection. My thesis project is based on the utilization of a murine infection model and Tn-seq, a high-throughput genetic technique, to identify Mtb counter-immune mechanisms. This project has the potential to provide information that can be utilized in the development of TB vaccines and therapies.