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- 2026 Prize Finalist Zuri Sullivan, Ph.D.
2026 Prize Finalist Zuri Sullivan, Ph.D.
Member of the Whitehead Institute for Biomedical Research, Whitehead Career Development Professor of Biology at MIT, and HHMI Hanna H. Gray Faculty Fellow
Her research spans microbial pathogenesis, immunology, and neuroscience to understand host defense across biological scales. She began studying Mycobacterium tuberculosis at Harvard, then moved to Durban, South Africa as a Fulbright Scholar to study human immunity to HIV and tuberculosis. At Yale, in Ruslan Medzhitov’s laboratory, she investigated how immunity regulates intestinal physiology. As an HHMI Hanna H. Gray Fellow in Catherine Dulac’s laboratory at Harvard, she studied how the brain responds to immune threats. Her laboratory now investigates sickness as an integrated, organism-wide host defense program.Essay: “Immunity, at scale”
Host defense operates at many biological scales, from antimicrobial programs within individual cells to coordinated responses across tissues. Zuri Sullivan’s research asks how immunity extends to the scale of the whole organism through sickness – the reorganization of temperature, appetite, sleep, activity, and social behavior that accompanies infection. By comparing bacterial, viral, and parasitic infection, allergy, and colitis in mice, she found that different immune challenges produce distinct physiological and behavioral states. Brain-wide activity mapping showed that these sickness states are also represented differently in the brain: activity in a small set of regions could predict the animal’s peripheral immune state. Spatial transcriptomics further revealed distinct, cell-type-specific molecular responses in the hypothalamus. Together, this work shows that the brain monitors immune state with unexpected specificity and reframes sickness as an integrated component of host defense – immunity at the organismal scale. Her laboratory now builds on this framework to ask how the brain generates sickness during live infection and how sickness itself shapes host-pathogen interactions.
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