Associate Professor of Medicine
Division of Gastroenterology and Hepatology
| Address: | 1825 University Blvd Shelby Building, 672 UAB Birmingham, AL 35294 |
| Telephone: | 205-975 9244 |
| FAX: | 205-996-9113 |
| Email: | rshen@uab.edu |
| Publications |
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Education
B.S. (Virology), Wuhan University, Wuhan, P.R. China
Ph.D. (Genetics), Iowa State University, Ames, IA
Research Interests
Early mucosal HIV-1 Infection. Mucosal surfaces play a major role in HIV-1 transmission and pathogenesis. Virtually all human immunodeficiency virus type 1 (HIV-1) infections, excluding those acquired parenterally, are acquired via the mucosal surfaces of the genital or the gastrointestinal tracts. However, the immediate events between exposure to infectious virus and establishment of infection are poorly understood. We seek to define the biological parameters of HIV-1 entry, infection, and dissemination in genital and gut mucosae. Our current focus includes HIV-1 transcytosis across epithelium, identification of first target cells in mucosae, and the selective entry and transfer of macrophage-tropic HIV-1. A better definition of these early steps in mucosal transmission is necessary in order to develop successful HIV-1 vaccines.
Mucosal macrophages in HIV-1 Pathogenesis. Although the mucosa is the largest reservoir of macrophages in the body and mucosal macrophages play an important role in host defense, studies of monocytes/macrophages in HIV-1 infection have focused on blood monocytes and lymph node macrophages, which have been implicated in the establishment, persistence and pathogenesis of HIV-1 infection. However, the striking and well defined phenotypic and functional differences between blood monocytes and mucosal macrophages preclude the simple extrapolation from findings in HIV-1-infected monocytes to HIV-1 infection of mucosal macrophages. We seek to elucidate the roles of mucosal macrophages in the pathogenesis of HIV-1 infection using purified macrophages from human genital and gut mucosal tissues. Current focus includes the mechanisms of down-regulation of HIV-1 infection in intestinal macrophages and the HIV-1 permissiveness of genital and gut macrophages.