David S. Weiss, PhD

Associate Professor

Emory Vaccine Center

Assistant Professor

Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine


Yerkes National Primate Research Center

Phone: 404-727-8214

Fax: 404-727-8199

Email: david.weiss@emory.edu

Additional Contact Information


Dr. Weiss received his PhD degree 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.

Research Interests

Our lab studies the interaction of bacterial pathogens with the host, focusing on Francisella tularensis, a potential bioweapon, and Acinetobacter baumannii, a highly antibiotic-resistant, hospital-acquired pathogen.

F. tularensis is one of the most highly virulent intracellular bacterial pathogens and causes the potentially lethal disease tularemia.  Tularemia can kill up to 60% of those infected, with an infectious dose estimated to be less than 10 bacteria.  Unfortunately, relatively little is known about which genes F. tularensis uses to subvert host defenses.  Studying how Francisella efficiently subverts innate immune defenses is critical to understanding not only tularemia, but also the virulence strategies of other bacterial pathogens that employ similar mechanisms of immune evasion.  We are currently characterizing novel F. tularensisvirulence genes that were previously identified in an in vivo negative selection screen as being essential for replication and survival during murine infection.  We have thus far elucidated the function of an organic hydroperoxide resistance protein, a novel biotin biosynthetic protein that revealed a link between metabolism and phagosomal escape, two proteins involved in lipid A modification and resistance to host antimicrobials, and a protein required for repression of bacterial lipoprotein (BLP) levels and evasion of the host innate immune receptor TLR2.

A. baumannii is an increasing cause of hospital-acquired, extensively antibiotic-resistant infections.  Polymyxin antibiotics are currently the “last line” drugs to treat this pathogen, but increasing numbers of clinical isolates are even resistant to these antibiotics.  We have identified novel genes that facilitate A. baumannii antibiotic resistance, and are utilizing this knowledge to design therapeutics to reverse resistance.  We are also studying how this pathogen evades innate defenses to establish infection, and working to develop a novel vaccine to treat antibiotic-resistant infections.