While there are currently drugs available to treat patients with human immunodeficiency virus (HIV), there is no known cure for this infection. As the HIV virus integrates into the host’s DNA, reservoirs of latent HIV are established. Because antiretroviral drugs only attack replicating HIV, the presence of these latent reservoirs prevents the eradication of the virus from the body. Once the use of anti-retroviral drugs is discontinued, the active virus reemerges in patients. The purpose of this project is to identify transcriptional and epigenetic pathways to reverse HIV latency, knowledge that could pave the way for new drug design to kill all existing virus in the body. To accomplish this goal, we are using a microplate-based matrix chromatin immunoprecipitation (ChIP) assay and quantitative polymerase chain reaction (qPCR) to measure more than one hundred different transcription and epigenetic events along the latent HIV genome upon its transcriptional activation. We applied cluster analysis to our data and have found that Protein Kinase A (PKA), a class of enzymes which phosphorylate proteins, and its target, the transcriptional factor CREB, are recruited to HIV genome. This finding, which has not previously been reported, suggests that PKA plays a role in HIV genome transcription, and if so, could be a possible path for developing pharmacological reversal of HIV latency.