Wendy J. Maury, Ph.D.
Ph.D., University of Virginia, 1988 |
Associate Professor of Microbiology Campus address: 3-612 BSB Mailing address: 51 Newton Rd. 3-612 Bowen Science Building Iowa City, IA 52242 Phone: 319-335-8021 Email: |
Regulation of enveloped virus entry and pathogenesis
A goal of our research is to understand how enveloped viral glycoproteins bind to and enter permissive cells. An appreciation of the cellular attachment factors, receptors and subsequent internalization pathways used by a virus to enter cells provide an avenue for the development of antiviral therapies. To this end, my laboratory studies two related lentiviruses, human immunodeficiency virus (HIV-1) and equine infectious anemia virus (EIAV) as well as the filoviruses, Ebola and Marburg. Our recent studies have helped to elucidate the endosomal pathway used by EIAV and filoviruses for entry and identified Ebola glycoprotein amino acids that are critical for Ebola virus internalization. Several different approaches are currently being developed within the lab to block the entry of these viruses into target cells.
As a twist on this same theme, we have used the knowledge gained from our studies on virus glycoproteins to develop more efficient vectors for the delivery of therapeutic genes. A number of viral glycoproteins such as Ebola virus broadly enter a variety of different host cells and will readily incorporate onto the surface of viral vectors that can be used to deliver gene therapy. Through the identification of viral glycoprotein motifs that are important for mediating entry into cells, we are developing better viral vectors for genetic diseases such as cystic fibrosis and hemophilia A.
Finally, in a related project on lentiviruses, the inhibitory activities against lentiviruses of constituents of three important medicinal plant genera, Echinacea, Hypericum and Prunella, are being explored.
Additional Information
UI Carver College of Medicine Interview
Recent publications
Brindley, M.A., B. Zhang, R. Montelaro, and W. Maury. 2008. An equine infectious anemia virus variant superinfects cells through novel receptor interactions. Journal of Virology (in press).
Tallmadge, R.L., M.A. Brindley, J. Salmans, R.H. Mealey, W. Maury, and S. Carpenter. 2008. Development and characterization of an equine infectious anemia virus Env pseudotyped reporter virus. Clinical and Vaccine Immunology 15:1054-1059.
Brindley, M.A., and W. Maury. 2008. Equine infectious anemia virus entry occurs through clathrin-mediated endocytosis. Journal of Virology 82:1628-1637.
Sinn, P.L., J.D. Goreham-Voss, A.C. Arias, M.A. Hickey, W. Maury, C.P. Chikkanna-Gowda, and P.B. McCray, Jr. 2007. Enhanced gene expression conferred by stepwise modification of a nonprimate lentiviral vector. Hum Gene Therapy 18:1244-1252.
Biglione, S., S.A. Byers, J.P. Price, V.T. Nguyen, O. Bensaude, D.H. Price, and W. Maury. 2007. Inhibition of HIV-1 replication by P-TEFb inhibitors DRB, seliciclib and flavopiridol correlates with release of free P-TEFb from the large, inactive form of the complex. Retrovirology 4:47.
Brindley, M.A., L. Hughes, A. Ruiz, P.B. McCray, Jr., A. Sanchez, D.A. Sanders, and W. Maury. 2007. Ebola virus glycoprotein 1: identification of residues important for binding and postbinding events. Journal of Virology 81:7702-7709.
Brindley, M.A., and W. Maury. 2005. Endocytosis and a low-pH step are required for productive entry of equine infectious anemia virus. Journal of Virology 79:14482-14488.