Research interests
Viral translation and host defense
Viral translation and host defense
Viral translation and host defense
For RNA viruses, translation must occur before the replication cycle begins. We investigate how viral RNAs gain access to host ribosomes, how infection remodels the translation environment, and how cellular defense mechanisms act on translating viral RNA.
These studies seek to understand why the same viral RNA can lead to different disease in different cell types and how those differences influence infection.
Translation in neurodegeneration
Viral translation and host defense
Viral translation and host defense
Disruption of protein synthesis can itself become a source of cellular stress. Our work in Huntington's disease revealed that mutant Huntingtin perturbs ribosome function, protein homeostasis, and stress responses.
We investigate how altered translation, protein biogenesis, and protein-protein interactions contribute to neuronal dysfunction and whether manipulating these processes can change disease outcomes.
From mechanism to intervention
Viral translation and host defense
From mechanism to intervention
Mechanistic understanding creates opportunities to engineer biological outcomes. Current work applies principles of translational control to develop viruses whose protein synthesis is selectively restricted in vulnerable cell types, providing a potential new layer of attenuation for safer vaccines.
Across infection and neurodegeneration, we aim to convert translational control from a disease mechanism into an intervention.