In the Weinberger lab, I plan to investigate how the human immunodeficiency virus (HIV) can hide quietly inside host cells, emerging when conditions are most favorable. When HIV infects a human immune cell, it can choose to replicate aggressively, producing many viral copies—or it can enter a period of suspended animation, or latency. The virus can remain in this dormant state for decades, evading detection by the immune system or elimination by antiviral therapies. But some HIV-infected latent cells will periodically “test the waters” by briefly switching replication on—an approach that allows the virus to emerge in force once treatments are interrupted. Using techniques in molecular biology, virology, mathematical modeling, and live-cell imaging, I will explore how random fluctuations in the production of a regulatory protein called Tat influences HIV’s ability to switch between latency and replication. By manipulating the synthesis and stability of Tat—which strongly stimulates viral replication—I will determine whether a buildup of this regulator keeps HIV from entering its latent state. The results could lead to innovative strategies for eradicating viral reservoirs and treating HIV and AIDS.