Solving the biology
of Chlamydia
pathogenesis

We are broadly interested in elucidating the cell and molecular biology of Chlamydia–host interactions — specifically the strategies used by Chlamydia to control host signaling pathways and cell function. This work encompasses both target-based experimentation and large-scale proteomic strategies.

We have investigated Chlamydia entry and exit mechanisms in detail. Our investigations of chlamydial exit mechanisms helped establish a new paradigm for understanding chlamydial cell-to-cell spread within a host, demonstrating two distinct pathways: lysis and extrusion.

Through structure-function analysis in collaboration with Scott Hefty, Scott Lovell, and the Seattle Structural Genomics Center for Infectious Disease, we are working to discover the structures and functions of the large pool of uncharacterized hypothetical proteins encoded by C. trachomatis.

Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infection worldwide. We are increasingly interested in connecting our molecular and genetic findings to the context of real human infections.

We explore this on three fronts: whole genome sequencing to identify genetic factors governing host tropism at distinct mucosal sites; determining human immunological correlates of protection and clearance; and using a peptide-based assay to perform molecular serology on patient sera.

This translational work is central to our long-term goal of informing vaccine and therapeutic development for a pathogen that disproportionately affects young women and people from disadvantaged backgrounds.