Many viruses increase the DNA content (ploidy) of infected host cells. Given the profound changes in biology caused by ploidy increases, we are interested in identifying the roles that polyploidy may play in diseases caused by such viruses. Our current efforts in this area involve a collaboration with Dr. Mary Klotman's laboratory, on the role of polyploidy in the HIV-infected kidney.
Previously, work from the Klotman laboratory identified polyploidy as a recurrent cellular property in biopsies of HIV+ individuals . Work in cultured renal cells and mouse models identified the HIV Vpr protein as the key player in HIV-induced renal polyploidy. Similarly, in CD4+ T cells, it was shown that Vpr expression can cause a large fraction of cells to become polyploid. Our current work seeks to identify targetable changes in polyploid HIV+ cells, and to understand the molecular events (and their significance) that generate polyploidy after HIV infection.