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The Weinberger Lab at the University of Miami Miller School of Medicine studies the fundamental principles that govern cell-fate decisions and uses them to rationally target fate-regulating circuits for therapeutic benefit. Led by Leor S. Weinberger, Ph.D., Professor and Founding Chairman of the Department of Cell and Systems Biology, the lab brings together quantitative virologists, biologists, and theoreticians to decode how viruses select between alternate fates and to translate those rules into next-generation antiviral therapies.
Our central question is deceptively simple: how does a biological system choose one fate over another? To answer it, we couple mathematical methods with wet-lab experiments, moving between theory and the bench to identify the core regulatory principles that govern fate selection in viruses and developmental systems. This dual approach lets us find the control points that drive these decisions rather than just describing them.
We use viral pathogens as our model systems because they make these decisions under pressure. Pathogenicity creates inherent fitness trade-offs, since a virus must balance transmission against virulence. One strategy viruses have evolved to manage that tension is bet-hedging between active and latent states. Because viruses are genetically constrained and favor minimalist regulatory circuits, they are ideal for isolating the core principles behind biological bet-hedging decisions. Much of our foundational work has centered on two viruses, HIV and human herpesvirus 5, also known as cytomegalovirus (CMV).
Over the past two decades, this focus has produced a series of discoveries that span fundamental biology and new therapeutic strategies. A common thread runs through all of it: the interplay of molecular noise and feedback in determining cell fate. That insight has reshaped how fate decisions are understood, from viral latency to embryonic cell transitions, and revealed regulatory rules that recur broadly across biology rather than in viruses alone.
These discoveries point us toward therapy. By treating fate-regulating circuits as drug targets, we work to develop a distinct class of interventions, including noise-modulating compounds, escape-resistant antivirals, and adaptive therapies designed to co-evolve with their target. The goal is a set of antiviral strategies that holds up against the very trade-offs viruses use to survive.