|Contact Information |
Phone: (404) 752-1862
Fax: (404) 752-1047
B.S., Pennsylvania State University, University Park, PA (Biology)
M.S., Pennsylvania State University (Genetics)
Ph.D., Pennsylvania State University (Genetics)
My laboratory's research goal is to further our understanding of host-HIV-1 interactions and the role, if any, this plays in progression to AIDS. We have focused our efforts on the role(s) played by extracellular HIV-1 proteins in the pathogenic manipulation of host systems.
- It has been proposed that T lymphocyte depletion is a result of cell killing (apoptosis) predominantly in uninfected or "bystander" cells, with a distinct lack of cell killing in the productively infected cells themselves. Although a number of viral factors, including HIV-1 Nef, have been implicated in protecting infected cells, it is not clear what factor(s) are important in bystander cell killing. We have focused our efforts on an examination of the role of extracellular Nef protein in pathogenicity leading to peripheral lymphocyte depletion, and the onset of AIDS.
- Endothelium plays a key role in disease containment as well as disease progression, while simultaneously representing a potential target for immunomodulation. Clinical data clearly suggest expression changes as well as structural changes in endothelium in HIV-1 infected individuals. However, what role endothelium plays in HIV-1 pathogenesis, is not well understood. We are examining the molecules, mechanisms, and signaling underlying HIV-1 gp120-induced activation and apoptosis in endothelium.
- The differential susceptibility of different individuals within a population to HIV-1 infection suggests that host-related genetic factors play an important role in HIV-1 transmission. We have identified one gene variant of human leukocyte antigen-G (HLA-G) that modulates vertical transmission in HIV-1 infected pregnant women. Studies are ongoing to further analyze HLA-G for its role in vertical transmission.
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