Using -omics to study the evolution of papillomavirus disease
Vaccines prevent new HPV infections. They do not help the millions of people already persistently infected. We want to close that gap with a direct treatment for persistent infection, before it becomes cancer.
To understand how HPV persists inside its host, and to turn that understanding into treatments for persistent infection before it becomes cancer.
Our lab studies how viruses and host genes evolve, using a combination of evolutionary genomics, single-cell sequencing, and engineered tissue models.
Our primary focus is cancer-causing human papillomaviruses (HPVs), responsible for an estimated 5% of cancers worldwide. To cause cancer, HPV must persist inside its host for months to years; acute infection alone is not enough. This creates a paradox at the heart of our work: when HPV triggers cancer, it destroys the very cellular machinery it depends on to replicate. We believe cancer is not the virus's goal, but a side effect of its drive toward long-term persistence. Understanding how that persistence is established is the path toward therapies that do not yet exist.
We also apply these same evolutionary and genomic tools outside of HPV, studying how the CD4 co-receptor evolved to regulate T cell activation by reconstructing hundreds of millions of years of CD4 evolution.
Explore our current projects to see this work in detail.