The effect of a specific Heat Shock Protein 90 inhibitor on HIV-1 infection



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This thesis describes the effort to characterize several intracellular signaling and transport molecules during HIV-1 infection via chemical inhibition. Many pharmaceutical molecules developed for one purpose find a second or third life in the treatment of another medical condition. The cellular changes resulting from cancer in some cases resemble changes in signaling which occurs during HIV-1 infection. During the course of this research, several pathways of signaling were variously knocked down, or otherwise inhibited using multiple methods to determine if one or more already-developed chemical compounds could be useful in the treatment or study of HIV-1 disease. During the course of this research and writing, the author conducted numerous literature searches and laboratory investigations to develop the evidence necessary to demonstrate one cell-signaling pathway that is vital to viral infection. The inhibition of the heat shock protein 90 protein leads to the conclusion that tanespimycin impacts viral infection in the described models.