Research
Viruses are parasites and can't build everything they need, so they hijack the host cell. I study where that dependence becomes a weakness.
Pan-antivirals that can be deployed quickly in the face of an epidemic remain a major unmet need and is a gap the COVID-19 pandemic made impossible to ignore. My research in the Arias Group at Biohub (San Francisco) explores the molecular mechanisms of virus–host interactions in cells infected with medically relevant viruses.
The goal is to reveal host dependencies that can be targeted for broad-spectrum antiviral interventions: cellular factors that viruses lean on to meet their unusually high biosynthetic demands, but that the cell itself can briefly do without. Subtle changes to these factors may impair viral replication without harming the host.
A standardized CRISPRi platform interrogating >3,000 proteostasis-network genes across three DNA viruses: HSV-1, HCMV, and Vaccinia. Iterating from survival-based to quantitative FACS readouts to pull out the host dependency factors that viruses share.
From screen hit to mechanism: a small-molecule retrograde-transport inhibitor with antiviral activity validated across multiple viruses, including herpes- and poxviruses. Characterizing differential drug mechanisms with quantitative cell assays and mass spectrometry.
V-SWITCH: a single-vector OFF-to-ON fluorescent reporter of live RNA-virus infection, paired with single-cell image-analysis pipelines (Cellpose segmentation, Ultrack tracking, ML classification) to resolve infection dynamics one cell at a time.