Nearly every cell in the human body has the capacity to detect viral infection and sound an “alarm”, inducing a potent antiviral state in uninfected cells. Perhaps unsurprisingly, viruses have evolved a number of mechanisms to evade, or otherwise co-opt, this antiviral response. Regardless in a few, precocious, cells, our body inevitably overcomes viral antagonism and manages to mount a response. My lab studies these rare events that define the subsequent immune response, particularly in the context of an important human pathogen, influenza. We use a multidisciplinary approach, leveraging single cell transcriptomics/genomics, flow cytometry, population-level sequencing, and fine-grained genetic analysis to explore the following concepts:

1. How does variation in viral populations drive the resultant innate immune response?

2. What cellular features control the rarity of interferon induction? How do they change as infection progresses?

3. Can we leverage our knowledge of these processes to develop improved therapeutic interventions and vaccine candidates?