Abstract
HIV is incurable due the persistence of latent but replication competent HIV proviruses. Lifelong antiretroviral therapy (ART) stops HIV progression to AIDS with minimal side effects. However, a HIV cure has only been achieved in rare cases with stem cell transplants. Multiple epigenetic mechanisms dictate the chromatin environment at the HIV integration site which in turn dictate HIV transcription and latency. In this thesis I will explore how histone marks, in particular histone citrullination, and the immune system affect HIV transcription and latency.
