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Jenny Hyde, PhD

Jenny Hyde
Jenny Hyde, PhD

Associate Professor

Contact

Microbial Pathogenesis & Immunology
8447 Riverside Pkwy
Bryan, TX 77807
jhyde@tamu.edu
Phone: 979.436.0872
Fax: 979.436.0360

Education and Training

  • Texas A&M University , BS, 2000
  • Texas A&M University Health Science Center, PhD, 2005
  • Texas A&M Health Science Center, Postdoctoral, 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 the CDC reporting over 300,000 cases per year. Lyme disease progresses in multiple stages that includes early or localized, disseminated, and late stages. Localized disease occurs after an infected deer tick (Ixodes) transmits B. burgdorferi into the skin while feeding on a small rodent, bird, dog, or human. At this stage patients may experience general flu-like symptoms and approximately 70% will develop a characteristic bulls-eye rash, also known as erythema migrans. In the absence of antibiotic treatment, the pathogen disseminates and colonizes secondary tissues, such as the heart, central nervous system, and joint, that may develop into Lyme carditis, Neuroborreliosis, of Lyme arthritis, respectively. B. burgdorferi causes a highly inflammatory disease with patients experiencing chronic and severe morbidity. Serodiagnostic tests that measure borrelial antibodies are recommended by the CDC and will diagnose later stages of disease. Currently, a diagnostic for early Lyme disease or a human vaccine is not available.
  • B. burgdorferi undergoes dynamic genetic regulation to survive and persist in the tick vector and mammalian reservoir. With a minimal genome lacking in metabolic pathways and pathogenic mechanisms B. burgdorferi is able to withstand the host immune response and adapt to vastly distinct environments. The focus of my research is to identify and characterize the host-pathogen interactions of B. burgdorferi in both the tick vector and mammalian host. We approach this in three ways: 1) Identifying borrelial genetic mechanisms required for distinct stages of disease and the development of inflammation, 2) Characterizing the immune response induced by B. burgdorferi and how it supports pathogenesis, 3) Elucidate the virulence factors important for transmission, colonization, survival, and persistence within the tick vector. We employ a wide variety of molecular and genetic techniques to address these areas of interest. One unique tool utilized by my lab is in vivo imaging of bioluminescent B. burgdorferi to understand the progression of borrelial infection and genetic responses necessary for specific stages of disease and/or tissues.

Awards, Recognition and Service

  • 2023 JUNIOR FACULTY RESEARCH EXCELLENCE AWARD

Representative Publications

 

  • Farris LC, Torres-Odio S, Adams LG, West AP, Hyde JA. Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway. J Immunol. 2023 Jun 1;210(11):1761-1770. doi: 10.4049/jimmunol.2200354. PMID: 37067290; PMCID: PMC10192154.
  • Ante VM, Farris LC, Saputra EP, Hall AJ, O'Bier NS, Oliva Chávez AS, Marconi RT, Lybecker MC, Hyde JA. The Borrelia burgdorferi Adenylate Cyclase, CyaB, Is Important for Virulence Factor Production and Mammalian Infection. Front Microbiol. 2021 May 25;12:676192.
    doi: 10.3389/fmicb.2021.676192. PMID: 34113333; PMCID: PMC8186283.
  • Saputra EP, Trzeciakowski JP, Hyde JA. Borrelia burgdorferi spatiotemporal regulation of transcriptional regulator bosR and decorin binding protein during murine infection. Sci Rep. 2020 Jul 27;10(1):12534. doi: 10.1038/s41598-020-69212-7. PMID: 32719448; PMCID: PMC7385660.
  • Diana N. Medina-Pérez, Beau Wager, Erin Troy, Lihui Gao, Steven J. Norris, Tao Lin, Linden Hu, Jenny A. Hyde, Meghan Lybecker, Jon T. Skare (2020) The intergenic small non-coding RNA ittA is required for optimal infectivity and tissue tropism in Borrelia burgdorferi. PLOS
    Pathogens 16(5): e1008423. https://doi.org/10.1371/journal.ppat.1008423
  • James P. Phelan, Aurelie Kern, Meghan E. Ramsey, Maureen E. Lundt, Bijaya Sharma, Tao Lin, Lihui Gao, Steven J. Norris, Jenny A. Hyde, Jon T. Skare, Linden T. Hu. (2019) Genome-wide screen identifies novel genes required for Borrelia burgdorferi survival in its Ixodes tick vector.
    PLOS Pathogens 15(5): e1007644. https://doi.org/10.1371/journal.ppat.1007644
  • Hyde JA, Skare JT. Detection of Bioluminescent Borrelia burgdorferi from In Vitro Cultivation and During Murine Infection. Methods Mol Biol. 2018;1690:241-257. doi:10.1007/978-1-4939-7383-5_18
  • Hyde JA (2017) Borrelia burgdorferi keeps moving and carries on: A review on borrelial dissemination and invasion. Frontiers in Immunology 8:114. doi: 10.3389/fimmu.2017.00114.
  • Ramsey, M.E., Hyde, J.A., Medina-Perez, D.N., Lin, T., Gao, L., Lundt, M.E., Li, X., Norris, S.J., Skare, J. T., and L. Hu.  2017.   A high-throughput genetic screen identifies previously uncharacterized Borrelia burgdorferi genes important for resistance against reactive oxygen and nitrogen species.  
    PLoS Pathog. 13(2):e1006225
  • Skare JT, Shaw DK, Trzeciakowski JP, Hyde JA (2016) In Vivo imaging demonstrates that Borrelia burgdorferi ospC is uniquely expressed temporally and spatially throughout experimental infection. PLoS ONE 11(9): e0162501. doi: 10.1371/journal.pone.0162501
  • Hui Zhi, E.H. Weening, E.M. Barbu, J.A. Hyde, M. Höök, and J.T. Skare. 2015. The Borrelia burgdorferi BBA33 lipoprotein recognizes collagen and vitronectin and is essential for borrelial pathogenesis.  Mol. Microbiol. 96(1):68-83.
  • R.D. Gilmore, Brandt K.S. and J.A. Hyde. 2014. B. burgdorferi pncA and bptA are   insufficient to maintain Ixodes colonization and persistence in lp25 deficient background.  Infect. Immun. 82(12)  PMID:25245809
  • Shaw, D. K., Hyde, J. A., and J. T. Skare. 2011.  The Borrelia burgdorferi BB0646 protein is responsible for the lipase and hemolytic activity associated with the aetiological agent of Lyme disease.  Mol. Microbiol. 83(2):319-334.
  • Hyde, J.A., Weening, E.H., Chang, M.H., Höök, M., Cirrillo, J.D., and J. T. Skare.  2011. Bioluminescent imaging of Borrelia burgdorferi in vivo demonstrates that the fibronectin-binding protein BBK32 is required for optimal infectivity. Mol. Microbiol. 82(1):99-113.
  • 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, R., Trzeciakowski, J.P., and J. T. Skare.  2010. Characterization of a Conditional bosR Mutant in Borrelia burgdorferi. Infect. Immun. 78(1): 265-274***.  PMID: 19858309

                  ***Featured as a “Spotlight” Article in the January 2010 issue

  •  Hyde, J.A., Shaw, D.K., Smith, 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**.  PMID: 19906179

                       **A MicroCommentary accompanied this article