Daniel E. Voth, Ph.D.Associate Professor, Department of Microbiology & Immunology

Research Interest: Pathogenesis of Coxiella burnetii infection
Ph.D., University of Oklahoma, Norman, Oklahoma
Postdoctoral:  National Institutes of Health, Rocky Mountain Laboratories, Laboratory of Intracellular Parasites, Hamilton, Montana
Phone: (501) 686-8050
Fax:     (501) 686-5359


Research Description

The Voth laboratory studies Coxiella burnetii, an obligate intracellular bacterial pathogen that causes human Q fever.  Q fever generally presents as an acute debilitating influenzae-like disease. However, chronic infection can occur and normally manifests as life-threatening endocarditis.  In the host, Coxiella targets alveolar macrophages, wherein the pathogen directs formation of an intracellular replication vacuole with characteristics of host lysosomes.  Coxiella replicates to high numbers in this normally degradative compartment and produces proteins to manipulate its host cell throughout a lengthy infectious cycle.  Coxiella uses a Dot/Icm type IV secretion system (T4SS) to deliver bacterial proteins directly to the host cytoplasm where they can interact with a variety of host components to control infection.  We have identified multiple Coxiella proteins that are translocated by the Dot/Icm T4SS, a subset of which are encoded by genes on the pathogen’s endogenous cryptic plasmid.  We are using molecular biology, cell biology, and biochemistry techniques to identify host proteins that interact with Coxiella Dot/Icm substrates and define the host processes affected.  These studies will provide needed information about the arsenal of proteins used by Coxiella for successful parasitism of host cells.  We are also studying the impact of Coxiella infection on primary alveolar macrophage signaling.  We have found that Coxiella actively inhibits macrophage death during intracellular growth, in part, by activating the pro-survival host proteins Akt and Erk1/2.  Additionally, Coxiella activates numerous kinase pathways including cAMP-dependent protein kinase that are required for generation of its replication vacuole.  We are currently examining the role of kinase pathways in Coxiella infection and the pathogen proteins responsible for regulating kinase-dependent events.  Collectively, our studies will provide new insight into the complex interplay between intracellular bacterial pathogens and the host.


MacDonald, L.J., Graham, J.G., Kurten, R.C., and D.E. Voth. (2014) Coxiella burnetii Exploits Host cAMP-Dependent Protein Kinase Signaling to Promote Macrophage Survival.  Cellular Microbiology.  16:146-159.

Winchell, C.G., Graham, J.G., Kurten, R.C., and D.E. Voth. (2014) Coxiella burnetii Type IV Secretion-Dependent Interaction with Autophagosomes.  Infection and Immunity.  In press.

Graham, J.G., MacDonald, L.J., Hussain, S.K., Sharma, U.M., Kurten, R.C., and D.E. Voth (2013) Virulent Coxiella burnetii Pathotypes Productively Infect Primary Human Alveolar Macrophages. Cellular Microbiology. 15:1012-1025.

Maturana, P., Graham, J.G., Sharma, U.M., and D.E. Voth (2013) Refining the Plasmid-Encoded Type IV Secretion System Substrate Repertoire of Coxiella burnetii.  Journal of Bacteriology.  195:3269-3276.