My Research
undergraduate
My research journey began at Kent State University, where I completed my Honors Thesis with Dr. Gemma Casadesus in neuroendocrinology. I developed expertise in cellular localization and bioinformatics, producing a comprehensive atlas of the brain's production and distribution of luteinizing hormone that laid the groundwork for ongoing work in the lab.
As a trainee with BP-ENDURE at Washington University in St. Louis, I worked with Dr. Todd Braver to examine how genetic factors shape the neural activation patterns underlying cognitive control, using human fMRI. That work was published in Cerebral Cortex: Pattern Similarity Analyses of FrontoParietal Task Coding.
My curiosity about neurological disorders then led me to the Broad Summer Research Program at the Broad Institute of MIT and Harvard, where I worked with Dr. Beth Stevens on the role of the schizophrenia risk gene Csmd1 in synaptic pruning in the mouse cortex.
PhD
My PhD work in the Lehtinen Lab at Boston Children's Hospital and Harvard Medical School uncovered a new secretory mechanism in the choroid plexus (ChP), the epithelium that makes cerebrospinal fluid (CSF) — and showed that it shapes the CSF proteome and instructs cortical development.
Using live imaging, proteomics, and molecular profiling, I found that embryonic ChP epithelial cells release large packets of cytoplasm directly into the CSF through apocrine secretion, a calcium-dependent process triggered by serotonergic (5-HT2C) signaling. This changes what the neural progenitors lining the ventricles are exposed to, and shifts their developmental trajectory. Published in Nature Neuroscience: Choroid plexus apocrine secretion shapes CSF proteome during mouse brain development, with a companion mechanistic review in Fluids and Barriers of the CNS: Apocrine secretion by the choroid plexus.
I then asked what happens when this pathway is switched on by something a real pregnancy might encounter. Both maternal illness and psychedelics activate the embryonic ChP. In a follow-up study, I showed that maternal LSD crosses the placenta into embryonic CSF within minutes, drives apocrine secretion, and alters cortical lamination and adult offspring behavior in mice, identifying the choroid plexus as an embryo-facing interface that detects maternal drug exposure (preprint).
Working on this tissue also pulled me toward what happens when it fails. I wrote the Annual Review of Pathology survey of the field — Choroid Plexus Pathophysiology — covering the ChP's role in stroke, hydrocephalus, neurodegeneration, and infection. Writing it is what convinced me that the most interesting unanswered questions at this interface were immunological, and it is the most direct line between my thesis work and what I do now.
postdoc (present)
At Stanford, I study how hidden viral infections reshape the immune system and set chronic illness in motion. EBV infects nearly everyone, persists for life, and is increasingly implicated in autoimmune and neurological disease — but for any individual patient, we have had almost no way to see what the virus is actually doing, cell by cell.
In the Robinson Lab, I build the measurement first. I've developed computational and molecular methods that detect latent EBV in single cells from standard single-cell RNA-seq — without enrichment primers — and assign each infected cell to a viral latency program with statistical confidence. I pair this with EBV whole-genome sequencing and with paired B cell receptor data, to ask what those infected cells are targeting.
I apply these tools across multiple sclerosis, lupus, rheumatoid arthritis, and post-acute infection syndromes including Long COVID. Recent work from the lab: EBV reprograms autoreactive anti-CNS B cells as antigen presenting cells in multiple sclerosis.
The goal is to understand how an infection that most people clear without incident becomes, in some, the origin of decades of disease.
future
I'm building toward my own lab, and I intend to build it in Australia.
Latent viruses hide. Human herpesviruses including EBV, CMV, and HSV can sit in your cells for decades without announcing themselves, and in the data we usually collect they are effectively invisible — which means the question of what they're doing to people has stayed unanswerable rather than unasked.
I build the tools that make them visible, and my lab will keep doing that: methods that find latent virus in single cells, that say which cells are infected and what the virus is doing inside them, and that are validated well enough for other people to trust and reuse.
Then I'll point them at the diseases where the answer matters most:
Post-acute infection syndromes. Post-mono fatigue, Long COVID, post-Q-fever illness. Why do some people never fully recover?
Autoimmunity. Multiple sclerosis, lupus, rheumatoid arthritis — where EBV keeps turning up and nobody can yet say why.
Neurodegeneration. Herpesviruses persist in human tissue for a lifetime. Whether that persistence drives dementia is one of the biggest open questions in the field, and it stays open in part because it has been unmeasurable.