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The Paintsil laboratory focuses on increasing our understanding of the host determinants of individual differences in response to antiretroviral therapy; biomarkers of pathogenesis and the increasing incidence of cancers in HIV treatment-experienced individuals. The research interest was fostered by an NIH career development award (K08) from 2008 to 2013. During this period, studies identified the host determinants of individual differences in intracellular concentrations of antiretroviral drugs and the cellular kinases involved in the phosphorylation of nucleoside analogs, as well as the effects of treatment on mitochondrial function. Findings challenged the existing paradigm that nucleoside reverse transcriptase inhibitors (NRTIs) caused mitochondrial dysfunction by inhibition of mitochondrial DNA polymerase gamma (Pol-ɣ). The studies identified Pol-ɣ-independent pathways that lead to mitochondrial dysfunction, depletion of nucleotide pools, and mitochondrial DNA mutations. This led to the development of a novel hypothesis that ART causes mitochondrial dysfunction through both Pol-ɣ-dependent and Pol-ɣ-independent mechanisms, resulting in a decrease in cellular dNTP and rNTP pools, genomic instability, and clinical toxicity related to aging disorders in HIV-infected individuals.
GRE is optional for PhD applicants. TOEFL speaking scores below 26 or IELTS speaking below 7.5 may require summer English training.