David Strum Weiss, PhD

Associate Professor of Medicine

Emory University School of Medicine


Yerkes National Primate Research Center

Office: Yerkes Primate Center 2028

Phone: 404-727-8214

Fax: 404-727-8199

Email: dweiss8@emory.edu


Dr. Weiss received his PhD in Microbiology from New York University in 2004. Working under Dr. Arturo Zychlinsky, he studied how Toll-like Receptors work together to fight bacterial infections. He completed his postdoctoral training at Stanford University under Drs. Stanley Falkow and Denise Monack, studying virulence mechanisms of Francisella and the role of the inflammasome in host defense. He was the recipient of a three-year postdoctoral fellowship from the Giannini Family Foundation.

Our lab is interested in understanding mechanisms of bacterial pathogenesis and the host’s response to infection.

We are currently focusing on the Gram-negative bacterial pathogen Francisella tularensis. F. tularensis is highly infectious and causes tularemia, a potentially life-threatening disease in humans. Critical to Francisella’s pathogenesis are its ability to replicate within macrophages, the primary niche for replication in vivo, and to subvert the host immune system. Unfortunately, relatively little is known about which genes Francisella uses to modulate host defenses.

In order to identify critical Francisella virulence genes, we recently employed a powerful global in vivo negative selection screen. This approach resulted in the identification of 164 genes that are required for virulence, 44 of which appear to encode novel virulence factors. Study of mutants lacking two of the novel genes we identified revealed that they act to suppress the macrophage cell death response. We previously described that this pathway, dependent on the host inflammasome complex containing the proteins Caspase-1 and ASC, plays an important role in host defense against Francisella infection. This highlights how Francisella attempts to suppress critical host defenses, and the molecular tug-of-war that takes place between Francisella and the host during infection.

Future work will elucidate the roles of other novel Francisella virulence factors as well as identifying the host defense pathways that they modulate. One area of focus will be determining if and how Francisella subverts dendritic cell function to evade the immune response. Our work will allow us to gain insights into Francisella pathogenesis and host-pathogen interactions while leading us towards an F. tularensis vaccine and the identification of critical targets for therapeutics to treat tularemia.