Ever wondered why a simple cold can knock you out for days, leaving you exhausted, feverish, and craving nothing but your bed? It’s not just about the virus or bacteria invading your body—it’s about the intricate dance between your immune system, brain, and behavior. But here’s where it gets fascinating: what if these symptoms aren’t just side effects of fighting infection, but deliberate strategies your body employs to heal? This is the question driving the groundbreaking work of Zuri Sullivan, a newly appointed assistant professor in MIT’s Department of Biology and a core member of the Whitehead Institute for Biomedical Research. Sullivan stands at the crossroads of neuroscience, microbiology, physiology, and immunology, unraveling the mysteries of how our bodies respond to illness. In this interview, she dives into her research, her vision for future collaborations, and the provocative ideas reshaping our understanding of immunity.
Q: What exactly is immunity, and why do we experience sickness during an infection?
A: Immunity is often misunderstood as solely the body’s defense against pathogens, but it’s far more complex. Think of it in two parts: the direct attack on invaders, like deploying an army to fight off bacteria, and the systemic changes we call sickness—fatigue, fever, loss of appetite. Most people assume sickness is just collateral damage from the immune system’s battle, but I argue it’s an adaptive response. For instance, fever isn’t just discomfort; it’s a strategic move to create an inhospitable environment for pathogens. Similarly, losing your appetite might not be random—it could be your body conserving energy for healing. This interplay between the immune system and the brain is where my research thrives. I’m mapping how these cellular conversations trigger behaviors and physiological changes, treating sickness as a form of immunity at the organismal level.
And this is the part most people miss: sickness isn’t a bug; it’s a feature. But here’s the controversial bit—what if we’ve been viewing these symptoms as problems to suppress, rather than signals to decode? Could over-the-counter fever reducers, for example, be interfering with a natural defense mechanism? It’s a question worth debating.
Q: Which sickness behaviors intrigue you the most?
A: During my PhD at Yale, I studied how the gut processes nutrients and how the immune system maintains balance in response to diet. This sparked my fascination with the gut-immune-brain axis. Take loss of appetite, for instance. We have compelling evidence suggesting it’s not just a side effect but a survival tactic. Your body might be saying, ‘Don’t eat—let’s focus on fighting this infection.’ Sleep is another puzzle. We all know infections disrupt sleep, but why? Is it to redirect energy, or is there a deeper mechanism at play? I’m also obsessed with tracking these changes over time. Infections aren’t static—they evolve, and so does our response. This dynamic interplay means no two illnesses are identical, which makes it both challenging and thrilling to study.
Q: What kind of team are you building, and what collaborations excite you?
A: My lab is a melting pot of biology disciplines, united by one goal: understanding organism-wide responses to infection. I’m not looking for experts who fit a mold; I want creative thinkers who challenge assumptions. For example, I’m a microbiology enthusiast without formal training—I need collaborators who can fill those gaps. The Whitehead Institute’s commitment to interdisciplinary work is a dream come true. I’m already collaborating with Sebastian Lourido’s lab, exploring how Toxoplasma gondii manipulates social behavior—a project I’m eager to expand. I’m also inspired by Siniša Hrvatin’s work on the hypothalamus and torpor. My research focuses on the same brain region, as it controls behaviors like appetite, sleep, and body temperature during sickness. By studying how different pathogens—parasites, viruses, bacteria—trigger unique sickness states, we can ask bold questions: Are these responses universal, or tailored to the threat? And what does this tell us about human resilience?
Here’s the provocative question I’ll leave you with: What if sickness behaviors aren’t malfunctions but masterclasses in survival? Should we rethink how we treat symptoms, or even how we define health? Let’s debate this in the comments—I want to hear your take!
