UCLA

Viruses have evolved many ways to modulate host cell systems for their own replicative needs. Understanding the molecular mechanisms of how they achieve this is not only key to studying viral pathogenesis and infection treatment, but also a way to better understand the host systems. In this dissertation, I present two projects aimed at better understanding the host-viral interplay. First, we will explore HIV latency reversal and its broader implications. In Chapter 2, I introduce our discovery of a novel HIV latency reversing agent, NSC95397, from a screen and our attempts to characterize how it mechanistically affects latently infected cells. In Chapter 3, I further describe our efforts to characterize its mechanism and evaluate its potential as a therapeutic. While it is still unclear how NSC95397 can reactivate latent viruses, NSC95397 is an interesting opening to further study as a therapeutic since it can synergize with previously studied latency reversing agents that failed in vivo in a physiologically relevant context. The second project, presented in Chapter 4, focuses on the molecular interplay between host and viral proteins. Here, I describe how we start characterizing an important host factor, DCAF1, and how we set up a proximity labeling system to better understand the proteomic changes surrounding it during infection. Together, this will increase our understanding of host pathways involved in HIV latency and infection, as well as provide the foundation for novel avenues of studying and targeting viral infections.