Dr. Kenney’s research effort has been focused upon understanding the molecular regulation and pathogenesis of the human herpesvirus, Epstein-Barr virus (EBV). Her work in EBV spans a broad range of topics, including viral gene regulation, the effects of the virus on the host immune response, and the development of novel, EBV-targeted therapies for EBV-positive tumors. She has extensively studied the mechanisms by which both EBV immediate-early proteins, BZLF1 and BRLF1, activate the lytic form of viral infection. Her group discovered that BZLF1 preferentially binds to, and transcriptionally activates, the methylated form of its downstream target promoter, suggesting a unique and unexpected mechanism by which EBV overcomes the inhibitory effect of viral genome methylation. Her group has also shown how the two EBV immediate-early proteins alter the host cell environment in multiple different ways, including usurping control of the host cell cycle, activating a variety of signal transduction pathways, inhibiting p53 function, dispersing PML nuclear bodies, and attenuating the host innate immune response. Dr. Kenney is now translating the results of these basic molecular studies into the development of new, EBV-targeted therapies for EBV-positive tumors. Her group is also developing a new small animal model to study EBV pathogenesis in vivo.
Shannon Kenney, MD
1400 University Avenue
Madison, WI 53706
MD, Yale School of Medicine Lab Website:
Understanding the molecular regulation and pathogenesis of the human herpesvirus; Epstein-Barr virus (EBV)
Ryan, J. L., Shen, Y.-J., Morgan, D. R., Thorne, L. B., Kenney, S. C., Dominguez, R. L., and Gulley, M. L. Epstein-Barr Virus Infection Is Common in Inflamed Gastrointestinal Mucosa. Dig. Dis. Sci., 57: 1887-1898, 2012.
Robinson, A. R., Kwek, S. S., and Kenney, S. C. The B-Cell Specific Transcription Factor, Oct-2, Promotes Epstein-Barr Virus Latency by Inhibiting the Viral Immediate-Early Protein, BZLF1. PLoS Pathog., 8(2):e1002516, 2012.
Ma, S.-D., Yu, X., Mertz, J. E., Gumperz, J. E., Reinheim, E., Zhou, Y., Tang, W., Burlingham, W. J., Gulley, M. L., and Kenney, S. C. An Epstein-Barr Virus (EBV) Mutant with Enhanced BZLF1 Expression Causes Lymphomas with Abortive Lytic EBV Infection in a Humanized Mouse Model. J. Virol., 86: 7976-7987, 2012.
Hagemeier, S. R., Barlow, E. A., Kleman, A. A., and Kenney, S. C. The Epstein-Barr Virus BRRF1 Protein, Na, Induces Lytic Infection in a TRAF2- and p53-Dependent Manner. J. Virol., 85: 4318-4329, 2011.
Hegde, S., Lockridge, J. L., Becker, Y. A., Ma, S., Kenney, S. C., and Gumperz, J. E. Human NKT Cells Direct the Differentiation of Myeloid APCs That Regulate T Cell Responses via Expression of Programmed Cell Death Ligands. J. Autoimmun., 37: 28-38, 2011.
Ma, S.-D., Hegde, S., Young, K. H., Sullivan, R., Rajesh, D., Zhou, Y., Jankowska-Gan, E., Burlingham, W. J., Sun, X., Gulley, M. L., Tang, W., Gumperz, J. E., and Kenney, S. C. A New Model of Epstein-Barr Virus Infection Reveals an Important Role for Early Lytic Viral Protein Expression in the Development of Lymphomas. J. Virol., 85: 165-177, 2011.
Robinson, A. R., Kwek, S. S., Hagemeier, S. R., Wille, C. K., and Kenney, S. C. Cellular Transcription Factor Oct-1 Interacts with the Epstein-Barr Virus BRLF1 Protein To Promote Disruption of Viral Latency. J. Virol., 85: 8940-8953, 2011.
Shaffer, D. R., Savoldo, B., Yi, Z., Chow, K. K. H., Kakarla, S., Spencer, D. M., Dotti, G., Wu, M.-F., Liu, H., Kenney, S., and Gottschalk, S. T Cells Redirected Against CD70 for the Immunotherapy of CD70-Positive Malignancies. Blood,117: 4304-4314, 2011.
Bristol, J. A., Robinson, A. R., Barlow, E. A., and Kenney, S. C. The Epstein-Barr Virus BZLF1 Protein Inhibits Tumor Necrosis Factor Receptor 1 Expression through Effects on Cellular C/EBP Proteins. J. Virol., 84: 12362-12374, 2010.
Hagemeier, S. R., Dickerson, S. J., Meng, Q., Yu, X., Mertz, J. E., and Kenney, S. C. Sumoylation of the Epstein-Barr Virus BZLF1 Protein Inhibits Its Transcriptional Activity and Is Regulated by the Virus-Encoded Protein Kinase. J. Virol., 84: 4383-4394, 2010.