All three of these proteins have been shown to be critical to HIV-1 replication and pathogenesis in vivo. In addition, these three viral gene products also use entirely novel mechanisms of action to enhance the level of viral replication. Each of these proteins therefore represents an attractive target from both the basic and applied research perspective. Removal of CD4 renders cells resistant to superinfection and may facilitate the release of HIV-1 virions by the infected cell. Current efforts in the laboratory are focused on identifying and characterizing the cellular co-factors for Tat and Rev function in vivo and on defining the mechanism by which Nef induces the specific internalization and degradation of CD4.
Students participate in all aspects of the research projects.
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