Stephen J. Davies, Ph.D.

Stephen J. Davies, Ph.D.

stephen davies

Name: Stephen J. Davies, BVSc., Ph.D.

Department of Primary Appointment: Microbiology & Immunology
Position: USU Faculty
Title: Associate Professor, MIC

Affiliated Departments: Molecular & Cell Biology, Emerging Infectious Diseases

Research Interests:
Immunology of Helminth Infections; Helminth Developmental Biology

Email: stephen.davies@usuhs.edu (link sends e-mail)
Office Phone: (301) 295-3446
Lab Phone: Fax: (301) 295-1545

Links
Department Website

Profile

Profile

B.V.Sc., University of Bristol School of Veterinary Science
Ph.D., Cornell University College of Veterinary Medicine 

Research

Molecular biology, biochemistry and developmental biology of helminth parasites and the immunobiology of helminth infections

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Figure 1: Scanning electron micrograph of a pair of Schistosoma mansoni

Helminths, or parasitic worms, including nematodes, flukes and tapeworms, collectively infect approximately 2 billion people worldwide, or about a third of the world population. The majority of infected people reside in developing countries in tropical and temperate climate zones, where helminths constitute a significant public health concern. Helminth infections are also of concern to U.S. service personnel, Peace Corps workers and civilians that visit these endemic areas. Many helminthiases are ancient diseases, recognized as scourges of humankind since antiquity, while others have risen to prominence recently and constitute emerging or re-emerging infections. Helminth infections can range from mild and unapparent to severe, with considerable morbidity and mortality, depending on the species of parasite involved and various other host and environmental factors.

Helminths are metazoans, with significantly larger genomes than other pathogens such as viruses, bacteria and protists. Consequently, helminths exhibit diverse cellular and molecular processes and complex developmental programs. Together, these features make helminths a challenging and exciting area of research and there is much to be learned about these important pathogens.

Schistosomiasis, caused by blood flukes of the genus Schistosoma, is a potentially serious case of liver, intestine and urinary system pathology that affects approximately 200 million people worldwide. Because efficacious vaccines for schistosomiasis have proved difficult to develop, the long-term objective of our studies is to develop new immunotherapies and chemotherapies aimed at inhibiting schistosome development in the definitive human host, thus simultaneously preventing the pathology associated with schistosome infection and blocking parasite transmission. Our previous studies, using a murine model of Schistosoma infection, have demonstrated that schistosomes require signals from host CD4+ T cells to complete their development normally, suggesting that blocking interactions between schistosomes and host T cells might provide a novel approach to interfering with parasite development. Currently we are focused on further understanding the role CD4+ T cells play in facilitating the development and reproduction of Schistosoma blood flukes and on elucidating how schistosomes respond to signals from the host immune system, from signal transduction to gene transcription.

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Figure 2: H&E-stained section of liver showing a juvenile Schistosoma mansoni developing in the portal venule of a wild type C57BL/6 mouse. Note the perivascular accumulations of lymphocytes, macrophages and eosinophils

Selected Publications

  • Fraga, L.A.O., Lamb, E.W., Moreno, E.C., Chatterjee, M., Dvorak, J., Delcroix, M., Sajid, M., Caffrey, C.R. and Davies, S.J. (2010) Rapid Induction of IgE Responses to a Worm Cysteine Protease During Pre-patent Schistosome Infection. BMC Immunology 11(1):56
  • Florin, D.A., Lawyer, P., Rowton, E., Schultz, E., Wilkerson, R., Davies, S.J., Lipnik, R., ad Keep, L. (2010) Population dynamics of Lutzomyia shannoni (Diptera: Psychodidae) at the Patuxent National Wildlife Research Refuge, Marlyand. J. Am. Mosq. Control Assoc. 26(3):337?339
  • Florin, D.A., Lawyer, P., Rowton, E., Schultz, E., Wilkerson, R., Davies, S.J., Lipnik, R., and Keep, L. (2010) Morphological Anomalies in Two Lutzomyia (Psathyromyia) shannoni (Diptera: Psychodidae: Phlebotominae) Specimens Collected From Fort Rucker, Alabama, and Fort Campbell, Kentucky. J. Med. Entomol. 47(5): 952-956
  • Lamb, E.W., Walls, C.D., Pesce, J.T., Riner, D.K., Maynard, S.K., Crow, E.T., Wynn, T.A., Schaefer, B.C., and Davies, S.J. (2010) Blood fluke exploitation of non-cognate CD4+ T cell help to facilitate parasite development. PLoS Pathogens 6(4):e1000892  * Selected for "Faculty of 1000 Biology"*
  • Swierczewski, B.E. and Davies, S.J. (2010) Conservation of protein kinase A catalytic subunit sequences in the schistosome pathogens of humans. Exp. Parasitol. 125(2):156-60
  • Swierczewski, B.E. and Davies, S.J. (2010) Developmental regulation of protein kinase A expression and activity in Schistosoma mansoni. Int. J. Parasitol. 40(8):929-35 
  • Fraga, L.A.O., Torrero, M.N., Tocheva, A.S., Mitre, E., and Davies, S.J. (2010) Induction of Type 2 Responses by Schistosome Worms During Pre-Patent Infection. J. Infect. Dis. 201, 464-472 
  • Swierczewski, B.E. and Davies, S.J. (2009) A Schistosome cAMP-Dependent Protein Kinase Catalytic Subunit is Essential for Parasite Viability. PLoS Negl. Trop. Dis. 3(8), e505 
  • Lamb, E.W., Crow, E.T., Lim, K.C., Liang, Y.-s., Lewis, F.A., and Davies, S.J. (2007) Conservation of CD4+ T cell-dependent developmental mechanisms in the blood fluke pathogens of humans. Int. J. Parasitol.37, 405-415 
  • Blank, R.B., Lamb, E.W., Tocheva, A.S., Crow, E.T., Lim, K.C., McKerrow, J.H. and Davies, S.J. (2006) The Common Gamma Chain Cytokines IL-2 and IL-7 Indirectly Modulate Blood Fluke Development Via Effects on CD4+ T cells. J. Infect. Dis. 194, 1609-1616