My lab is interested in understanding the molecular details of the relationship between host and pathogen responsible for tuberculosis (TB), the leading cause of death worldwide due to infectious disease. To begin to ask questions about TB pathogenesis, we have taken a molecular genetic approach to identify attenuated strains of Mycobacterium tuberculosis, the causative agent of TB. Initial results suggest that M. tuberculosis employs a number of unique mechanisms that make it a highly virulent and persistent pathogen. In particular, we are exploring the hypothesis that M. tuberculosis influences host-pathogen dynamics by utilizing the MmpL family of transporters to secrete biologically active lipids and polyketides to the surface of the mycobacterial cell and, ultimately, into infected host cells. This is an appealing hypothesis as many naturally occurring lipids and polyketides have potent biological activities and thus may alter host responses during infection. Our long-term research goals are to identify M. tuberculosis molecules important for virulence and to understand the role they play in the complex interactions between prokaryote and eukaryote. Ultimately, by understanding the details of TB pathogenesis at the molecular level, we hope to identify molecules that interfere with critical host-pathogen interactions that will aid in the discovery of new therapies to combat and eradicate this persistent infection.