PULSe Home > Faculty Members A-C > Erik Barton

Assistant Professor, Department of Biological Sciences Postdoctoral research, Washington University (2001-2006) PhD, Microbiology & Immunoloy, Vanderbilt University (2000) BA, Biology & Latin, Baylor University (1994) Click here to contact Dr. Barton Contact Info: 765-496-9688 Training Group(s): Molecular Virology

Current Research Interests:

Immunity during lifelong herpesvirus infection

The eight known human herpesviruses cause diseases including cold sores, blindness, chicken pox, infectious mononucleosis, and cancer. Herpesviruses are unique in their ability to persist in vivo in a non-replicating state referred to as latency, from which virus can periodically reactivate to produce infectious progeny and recurrent disease. Because of the capacity of these viruses to evade the immune response and remain with the person for life, these pathogens are the focus of intense immunologic research. However, it is still largely unclear how herpesvirus latency is maintained, and what the physiologic consequences of viral latency are for the infected cell and organism.

My lab uses the murine gammaherpesvirus 68 (gammaHV68) system to address these questions and improve our understanding of the immune response to latent herpesvirus infection. gammaHV68 is a natural pathogen of mice and is closely related to the human herpesviruses Epstein-Barr virus (EBV, which causes mononucleosis) and Kaposi's sarcoma herpesvirus (KSHV, which causes AIDS-associated tumors). The gammaHV68 model has four key advantages for studies of immunity to chronic virus infection: i) gammaHV68 can be easily mutated; ii) its genetic similarity to human herpesviruses has established it as a model system for exploring basic mechanisms of gammaherpesvirus infection, immunity, and cancer biology; iii) it encodes several genes that are predicted to modify cellular signaling pathways or evade the immune response; and iv) many knockout and transgenic mice with defined immune deficiencies are available, and novel mutant mice can be produced with relative ease.

My current research uses genetic and cell biological approaches to dissect mechanisms of immune function during gammaHV68 infection. I am specifically focused on understanding the role of interferons (a key antiviral cytokine family secreted during virus infection) in regulating latent virus infection, and the effects of prolonged interferon expression during latency on immune physiology. I seek to answer the following questions:

*How do interferons and other immune cytokines regulate herpesvirus gene expression and reactivation during latency?
*What host cells and cellular genes mediate the antiviral effects of interferon during herpesvirus infection in vivo?
*What viral genetic elements allow gammaherpesviruses to replicate, persist, and reactivate in the face of the interferon response?
*What are the long term consequences of herpesvirus latency for the host? Are there beneficial effects of latent infection that might indicate a symbiotic relationship between herpesviruses and their hosts?

Mentoring Philosophy:

My primary objectives as a mentor and teacher are:

1.To illuminate the diversity, complexity, and beauty of biological systems, using virology as a tool to dissect cellular biology and the host immune response.
2.To equip each student with analytical thinking skills with respect to the evaluation of data in context.
3.To emphasize the philosophical, ethical, and political context of biological research, including current controversies that affect funding, publication, application, and teaching in the biological sciences.
4.To foster the development of excellent teaching and public speaking skills in my students.
5.To help students gain a sense of their personal intellectual calling, and to become a lifelong mentor to guide them in that calling toward fulfilling and productive lives of their own design.

Selected Publications:

Barton, E. S., D. W. White, J. S. Cathelyn, K. A. Brett-McClellan, M. Engle, M. S. Diamond, V. L. Miller, and H. W. T. Virgin. 2007. Herpesvirus Latency Protects the Host from Bacterial Infection: Latency as Mutualistic Symbiosis. Nature 447:326-329.

Steed, A. L., E. S. Barton, S. A. Tibbetts, D. L. Popkin, M. L. Lutzke, R. Rochford, and H. W. Virgin. 2006. Gamma interferon blocks gammaherpesvirus reactivation from latency. J. Virol. 80:192-200.

Barton, E. S., M. L. Lutzke, R. Rochford, and H. W. t. Virgin. 2005. Alpha/beta interferons regulate murine gammaherpesvirus latent gene expression and reactivation from latency. J. Virol. 79:14149-14160.

O'Donnell, S. M., M. W. Hansberger, J. L. Connolly, J. D. Chappell, M. J. Watson, J. M. Pierce, J. D. Wetzel, W. Han, E. S. Barton, J. C. Forrest, T. Valyi-Nagy, F. E. Yull, T. S. Blackwell, J. N. Rottman, B. Sherry, and T. S. Dermody. 2005. Organ-specific roles for transcription factor NF-kappaB in reovirus-induced apoptosis and disease. J. Clin. Invest. 115:2341-2350.

Wang, F., Y. Ma, J. W. Barrett, X. Gao, J. Loh, E. Barton, H. W. Virgin, and G. McFadden. 2004. Disruption of Erk-dependent type I interferon induction breaks the myxoma virus species barrier. Nat. Immunol. 5:1266-1274.