Lyme disease, the most common vector-borne illness in the Northern Hemisphere and USA, is caused by the spirochetal pathogen Borrelia burgdorferi. Bacterial infection and dissemination culminates in a multisystem inflammatory illness with a broad spectrum of clinical manifestations including arthritis, carditis, and neuroborreliosis. B. burgdorferi is transmitted to humans through Ixodes ticks. To establish infection and to cause disease, B. burgdorferi must maintain its tick-mammal life cycle. It remains enigmatic how this recalcitrant pathogen interacts with ticks and animals to establish its persistence and cause tissue damages. Research in my laboratory is to understand how B. burgdorferi exploits complex genetic networks to decipher disparate tick and mammal signals and tailor its transcriptome, proteome, metabolome, and surface architecture for host adaptation.
