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Assistant Professor                                                                      


Contact Information:                                                                 
Email:
Office Phone: 318-675-4884
Laboratory Phone: 318-675-5111
Office Fax:  318-675-5764
                                                                                                           
Education/Training:
Postdoctoral Study, University of Washington/Seattle Children's Hospital
Ph.D., 1998, Bacteriology, University of Wisconsin-Madison
B.S., 1991, Biochemistry, University of Minnesota-Twin Cities

Major Research Interests:
Mechanisms of Pathogenesis of Group B Streptococcus

Group B Streptococcus (GBS) is an important pathogen for neonates and immunocompromised adults and can cause pneumonia, meningitis, and sepsis. However, relatively few virulence factors have been characterized for this pathogen. We are interested in the discovery and characterization of GBS virulence factors at the molecular level in order to understand how this bacterium causes disease. To accomplish this, we use the technologies of targeted gene knockout, in vitro and in vivo models for pathogenesis, and protein purification and characterization. One of the properties that contribute to GBS virulence is its ability to evade the innate immune system during an infection. We are characterizing an extracellular protease, CspA, that promotes virulence and resistance to the innate immune system. We are currently investigating the role the activity of this protease plays in contributing to virulence. A second research interest is the regulation of GBS virulence. During the infection process, GBS encounters a variety of different host environments and must adapt to these different conditions. It is our hypothesis that the two component transcriptional regulatory proteins encoded on the genome of GBS control its ability to transition between different environments. The analysis of GBS that harbor mutations in genes encoding these transcriptional regulatory proteins will give insight into how GBS adapts to host environment and how virulence factors are regulated. We have also characterized a transcriptional regulatory gene, MtaR, which is necessary for survival of GBS in vivo. We are currently determining what targets MtaR acts on and how it affects virulence.

Representative Publications:
Harris, T. O.*, Shelver, D. W.*, Bohnsack J. F., and Rubens, C. E. 2003. A novel streptococcal protease promotes virulence, resistance to opsonophagocytosis, and cleavage of human fibrinogen. J. Clin. Invest. 111: 61-70 *denotes authors contributed equally to this work.

Shelver, D. W., Rajagopal, L., Harris, T. O., and Rubens, C. E. 2003. MtaR, a regulator of methionine transport, is critical for survival of Group B Streptococcus in vivo. J. Bacteriology. 185:6592-6599.

Shelver D., Thorsteinsson, M.V., Kerby, R. L., Chung, S. Y, Roberts, G. P, Reynolds, M. F., Parks, R. B., and Burstyn, J.N. 1999. Identification of two important heme site residues (cysteine 75 and histidine 77) in CooA, the CO-sensing transcription factor of Rhodospirillum rubrum. Biochemistry 38: 2669-2678.

Shelver D., Kerby, R. L., He, Y., and Roberts, G. P. 1997. CooA, a CO-sensing transcription factor from Rhodospirillum rubrum, is a CO-binding heme protein. Proc. Natl. Acad. Sci. U S A. 1997:11216-20.

 


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