Jon Blevins, Ph.D.

Associate Professor
Department of Microbiology & Immunology 

Research Interest:  Pathogenesis and transmission of Lyme disease and relapsing fever Borrelia
Ph.D.: University of Arkansas for Medical Sciences, Little Rock, AR
Postdoctoral:  University of Texas Southwestern Medical Center, Dallas, TX 
 (501) 296-1253
Fax:  (501) 686-5359

Arkansas Tick-Borne Pathogen Surveillance Program

Research Description:
Pathogens belonging to the Borrelia genus are spirochetal bacteria transmitted to humans via the bite of an infected arthropod (e.g., ticks and lice).  There are two diseases, Lyme disease and relapsing fever, which are commonly associated with Borrelia infection in humans.  Despite intensive research efforts studying the Borrelia that cause Lyme disease and relapsing fever, there is still significant progress to be made towards understanding pathogenic mechanisms that these bacteria utilize to cause disease, colonize tick vectors, and transmit during tick feeding.  To address these knowledge gaps, we are working to determine how Lyme disease and relapsing fever Borrelia control the expression of their genes as they move between the tick and mammal and define contributions of individual Borrelia genes to bacterial virulence/infection and tick colonization.  One of the most direct approaches to demonstrate a causal relationship between a bacterial gene, its cognate gene product, and a requirement during the bacterial lifecycle is to create Borrelia strains in which specific genes of interest have been inactivated.  The abilities of these mutant strains to colonize animals and ticks can then be assessed experimentally to determine whether a given mutant is no longer competent for the phenotype of interest (e.g., infection, disease development, tick colonization, etc.).  Once we have identified bacterial factors that are required for Borrelia infection or tick transmission, we can begin to study their physiological contributions to these various bacterial processes.  In addition, since these bacterial factors are known to be essential during the bacterial lifecycle, they may also represent viable targets against which therapies could be developed to prevent, diagnose, or treat Lyme disease or relapsing fever.

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Current Lab Members:
Maple Guo, Graduate Student
Amber Atkinson, Research Technician

Clay Jackson-Litteken, Ph.D. (Graduate Student) – Postdoctoral Fellow, Washington University (Feldman Lab)

Jacob Latham, M.S. (Graduate Student) – Senior Microbiologist, Arkansas Department of Health

Danielle Graham, Ph.D. (Graduate Student) – Assistant Professor, Fayetteville State University

Ashley Groshong, Ph.D. (Graduate Student) – Unit Chief, Rocky Mountain Laboratories, National Institutes of Health

Tyler Ratliff, M.S. (Graduate Student/Research Technician) – UAMS College of Medicine

Marissa Fullerton, M.S. (Graduate Student/Research Technician) – UAMS Department of Microbiology and Immunology

Ember Fenton (Research Technician) – UAMS College of Pharmacy

Brendan Moore, M.S., M.D. (Research Technician) – UAMS Department of Emergency Medicine

Nora Gibbons, M.D. (Research Technician) – University of New Mexico Department of Family Medicine

Jackson-Litteken, C.D., Ratliff, C.T., Kneubehl, A.R., Siletti, C., Pack, L., Lan, R.S., Huynh, T.N., Lopez, J.E., and Blevins, J.S.  The diadenylate cyclase, CdaA, is critical for Borrelia turicatae virulence and physiology.  Infect Immun. 89:e00787-20.

Graham, D.E., Groshong, A.M., Jackson-Litteken, C.D., Moore, B.P., Caimano, M.J., and Blevins, J.S.  The BB0345 hypothetical protein of Borrelia burgdorferi is essential for murine infection.  Infect Immun.  88:e00472-20.

Jackson-Litteken, C.D., Zalud, A.K., Ratliff, C.T., Latham, J.I., Bourret, T.J., Lopez, J.E., and Blevins, J.S.  2019.  Assessing the contribution of an HtrA family serine protease during Borrelia turicatae mammalian infection.  Front. Cell. Infect. Microbiol. 9:290.

Brann, K.R., Fullerton, M.S., Onyilagha, F.I., Prince, A.A., Kurten, R.C., Rom, J.S., Blevins, J.S., Smeltzer, M.S., Voth, D.E. 2019. Infection of Primary Human Alveolar Macrophages Alters Staphylococcus aureus Toxin Production and Activity. Infect Immun. 20;87(7). pii: e00167-19.

Boyle, W.K., Groshong, A.M., Drecktrah, D., Boylan, J.A., Gherardini, F., Blevins, J.S., Samuels, D.S., and Bourret, T.J.  2019.  DksA controls the response of the Lyme disease spirochete Borrelia burgdorferi to starvationJ. Bacteriol. 201:e00582-18.

Caimano M.J., Groshong A.M., Belperron A., Mao J., Hawley K., Luthra A., Graham D.E., Earnhart C.G., Marconi R.T., Bockenstedt L.K., Blevins J.S., and Radolf J.D. 2019. The RpoS gatekeeper in Borrelia burgdorferi: an invariant regulatory scheme that promotes spirochete persistence in reservoir hosts and niche diversity. Front. Microbiol. 10:1923.

Latham, J.I. and Blevins, J.S.  2018.  Generation of conditional mutants in Borrelia burgdorferi.  Methods Mol. Biol. 1690:225-239.

Yin, Y., Yang, Y., Xiang, X., Wang, Q., Yang, Z., Blevins, J.S., Lou, Y., Yang, X.F., 2016.  Insight into the dual functions of bacterial enhancer-binding protein Rrp2 of Borrelia burgdorferi. J. Bacteriol. 198:1543–1552.

Wager, B., Shaw, D.K., Groshong, A.M., Blevins, J.S., and Skare, J.T.  2015.  BB0744 affects tissue tropism and spatial distribution of Borrelia burgdorferi.  Infect. Immun. 83:3693–3703.

Groshong, AM, Fortune, DE, Moore, BP, Spencer, HJ, Skinner, RA, Bellamy, WT, and Blevins, JS. 2014. The tetratricopeptide (TPR)-containing hypothetical protein, bb0238, is required during Borrelia burgdorferi mammalian infection.  Infect. Immun. 82:4292-4306.

Fortune, DE, Lin, Y, Deka, RK, Groshong, AM, Moore, BP, Hagman, KE, Leong, JM, Tomchick, DR, and Blevins, JS.  2014.  Identification of lysine residues in the Borrelia burgdorferi DbpA required for murine infection.  Infect. Immun.  Aug;82(8):3186-98.

Groshong, AM and Blevins, JS.  2014.  Insights into the biology of Borrelia burgdorferi gained through the application of molecular genetics.  Adv. Appl. Microbiol. 86:41-143.

Groshong AM, Gibbons NE, Yang XF, Blevins JS. 2012. Rrp2, a prokaryotic enhancer-like binding protein, is essential for viability of Borrelia burgdorferi. J Bacteriol.  Jul;194(13):3336-42.

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