Sarah Stubbs

Research Assistant Professor of Virology, Immunology & Microbiology

Research Interest

My research focuses on the molecular mechanisms that govern virus-host interactions for pathogens of high consequence with a particular emphasis on filoviruses.  Filoviruses are a family of negative-sense RNA viruses responsible for recurring outbreaks of severe disease, often with high mortality rates and limited therapeutic options.  Because viruses depend on host-cell machinery for replication, they must hijack and reprogram cellular processes to complete their life cycle.  At the same time, upon infection the host cell activates regulatory and antiviral pathways to restrict viral replication. My research examines both sides of this interaction: how filoviruses exploit host machinery, and how host defenses shape infection outcomes.

Within this broader framework, I am particularly interested in how viral infection interfaces with host RNA regulatory pathways. These pathways govern transcript stability, processing, localization, and translation, positioning them as key determinants of the cellular response to infection.  My work investigates how filoviruses disrupt these pathways to promote infection and how RNA quality-control mechanisms influence viral replication, the antiviral response, and virus-induced remodeling of the cell.

To address these questions, we integrate large-scale functional genomics, molecular virology, microscopy, and mechanistic cell biology.  These complementary approaches allow us to identify host factors important for infection and define their functions at the cellular and molecular levels.  Additionally, we use next-generation genomic technologies to define how filoviral infection reshapes the host transcriptome, including changes in transcript abundance, isoform diversity, alternative splicing, and RNA processing.

The continued emergence of filovirus outbreaks underscores the need for a deeper understanding of the cellular mechanisms that decide infection outcomes.  Identifying host factors and conserved cellular regulatory networks that promote or restrict infection is critical for understanding viral pathogenesis and uncovering new opportunities for therapeutic development.