Jenny Hyde
Jenny Hyde working in lab
Assistant Professor
Microbial & Molecular Pathogenesis
473 Reynolds Medical Bldg
College Station,
Texas 77843-1114
Phone: 979-845-0886
Fax: 979-845-3479
Email: jshyde@medicine.tamhsc.edu
Education and Post-Graduate Training
B.S., Microbiology, Texas A&M University (2000)
Ph.D., Texas A&M Health Science Center (2005)
Postdoctoral Fellow, Texas A&M Health Science Center (2005-2010)
Research Interests
Borrelia burgdorferi, the spirochetal bacterium that causes Lyme disease, is the most common tick-borne infection in the United States with over 35,198 cases reported in 2008. This value represented a 28% and 77% increase in incidence in the previous two years of reporting, respectively, indicating that Lyme borreliosis is a re-emerging disease. Early on, the infection is characterized by a skin lesion known as erythema migrans and a non-descript flu-like illness. Patients with untreated Lyme disease experience multisystemic symptoms with the arthritis being the defining indicator of long-term untreated infection.
The long-term objective of my research is to identify and characterized virulence determinants that contribute to the pathogenic potential of the B. burgdorferi. Through the utilization of in vivo bioluminescence we are evaluating the kinetics of borrelial infectivity in various strains or mutant derivatives that exhibit distinct phenotypes. We are also tracking how in vivo synthesis of critical virulence determinants affects B. burgdorferi colonization and dissemination. This work will contribute to the current body of knowledge by shedding light on the pathogenic and temporal role of specific borrelial genes during the infectious process.
Selected Publications
Hyde, J.A., Weening, E.H., and J. T. Skare. (2011) "Genetic Transformation of Borrelia burgdorferi." Curr Protoc Microbiol. Unit 12C.4.1-17.
Hyde, J. A., Shaw, D. K., Smith III, R., Trzeciakowski J. P., and J. T. Skare. (2010) "Characterization of a Conditional bosR Mutant in Borrelia burgdorferi." Infect. Immun. 78(1):265-274.* Publication was selected as editorial Spotlight for the issue.
Hyde, J. A., Shaw, D. K., Smith III, R., Trzeciakowski J. P., and J. T. Skare. (2009) The BosR regulatory protein of Borrelia burgdorferi interfaces with the RpoS regulatory pathway and modulates both the oxidative stress response and pathogenic properties of the Lyme disease spirochete. Mol. Microbiol. 74(6):1344-1355. * This publication was included in a Microcommentary.
Hyde, J. A., Trzeciakowski, J. P. and J. T. Skare. (2007) Borrelia burgdorferi alters its gene expression and antigenic profile in response to CO2 levels. J. Bacteriol. 189(2): 437-445.
Hyde, J. A., Seshu, J. and J. T. Skare. (2006) Transcriptional Profiling of Borrelia burgdorferi Containing a Unique bosR Allele Identifies a Putative Oxidative Stress Regulon. Microbiology 152(9): 2599-2609.
Seshu, J., Boylan, J. A., Hyde, J. A., Swingle, K. L., Gherardini, F. C. and J. T. Skare. (2004) A Conservative Amino Acid Change Alters the Regulatory Activity of BosR, the Redox Regulator of Borrelia burgdorferi. Mol. Microbiol. 54(5): 1352-1363.
