Elizabeth (Lee) Ann Fortunato, Ph.D.
College of Science
Campus Locations: Moscow
With UI Since 2000
Ph.D. Molecular Biology, University of California - San Diego, 1994
BS Applied Biological Sciences, Massachusetts Institute of Technology, 1986
Molecular and cellular biology
human cytomegalovirus host-pathogen interactions
Lee Fortunato has been an Associate Professor in the Biological Sciences department at the UI since 2007. She came here in 2000, after doing both her graduate and postdoctoral training at UC San Diego (and her BS at MIT). Lee's work involves the study of host (human)/pathogen (cytomegalovirus or HCMV) interactions. HCMV is a leading cause of birth defects. Those defects can dramatically impact the lives of the children (and their parents) that suffer from them. Lee's research is aimed at understanding the underlying mechanism for the development of those defects in order to someday prevent their occurrence. Lee has been continuously funded by the NIH since 2002 and has recently been appointed as a permanent member of the Virology B study section at the National Institute of Allergy and Infectious Diseases at the NIH.
- Casavant, N. C., M.H. Luo, K. Rosenke, T. Winegardner, A. Zurawska and E.A. Fortunato. 2006. potential role for p53 in the Permissive life cycle of human cytomegalovirus. J. Virol. 80: 8390-8401.
- Luo, M. H., K. Rosenke, K. Czornak and E.A. Fortunato. 2007. Human cytomegalovirus disrupts both ATM and ATR mediated DNA damage responses during lytic infection. J. Virol. 81: 1934-1950.
- Luo, M.H. and E.A. Fortunato. 2007. Long-term infection and virus shedding of human cytomegalovirus in T98G glioblastoma cells. J. Virol. 81: 10424-36.
- Luo, M.H., P. H. Schwartz and E.A. Fortunato. 2008. Neonatal neural progenitor cells (NPCs) and their neuronal and glial derivatives are fully permissive for human cytomegalovirus infection. J Virol. 82(20): 9994-10007.
- Hannemann H., Rosenke K., O’Dowd J.M. and E.A. Fortunato. 2009. The presence of p53 influences the expression of multiple HCMV genes at early times post infection. J Virol. 83(9): 4316-25.
- Luo M.H., H. Hannemann, A. Kulkarni, P.H. Schwartz, J. M. O'Dowd and E.A. Fortunato. 2010. Human cytomegalovirus infection causes premature and abnormal differentiation of human neural progenitor cells. J Virol. 84(7): 3528-41.
- Kulkarni, A.S. and E.A. Fortunato. 2011. Stimulation of homology-directed repair at I-SceI-induced DNA breaks during the permissive life cycle of human cytomegalovirus. J. Virol. 85(12): 6049-6054.
- Exploring the development of CNS defects in infants congenitally infected with HCMV. Studies in our lab focus on three important findings we have made regarding interactions with the host cell: 1) HCMV can inflict site-specific chromosomal damage to the host DNA; 2) HCMV dysregulates DNA repair in infected cells and 3) infection of neural progenitor cells by HCMV causes premature and abnormal differentiation of these important CNS cells. We hope to connect our observations in tissue culture to what occurs during development of the CNS in infected infants.
- Interactions of HCMV with the cell cycle regulatory protein p53. Studies in the lab have shown that: 1) HCMV interacts with p53 and sequesters it within the viral replication centers in the infected cell nucleus; 2) in those centers, p53 binds site-specifically to the viral genome and 3) infection of p53 knockout cells show dramatic decreases in viral titers, in viral DNA replication and in viral protein expression. Future work will continue to characterize the many areas where p53 plays a role in the HCMV life cycle.
- Participate as a mentor in INBRE program
- Lectured at Science on Tap events in Couer d’Alene and Moscow
- WWAMI UI/WSU-Site Teacher of the Year Award, 2003