The Levin lab studies the evolution of infectious diseases, seeking to understand how evolutionary “arms races” between hosts and pathogens dynamically shape the biology of immunity and pathogenesis. We approach these questions using a combination of high-throughput genetics, microbiology, and evolutionary genomics, focusing on the opportunistic pathogen Legionella pneumophila and its natural hosts, environmental amoebae. Our questions include:
- How do new opportunistic pathogens arise? Specifically, what sorts of host-microbe or microbe-microbe interactions select for these new pathogens to emerge?
- How do evolutionary arms races alter the molecular weaponry of pathogens, as well as the defensive strategies of hosts?
- How do new molecular mechanisms of immunity and pathogenesis arise?
To investigate these questions, we use Legionella bacteria and Dictyostelium amoeba hosts. Legionella pneumophila is an opportunistic bacterial pathogen of humans that causes outbreaks of a lethal, pneumonia-like illness called Legionnaires’ disease. Although human infections are evolutionary ‘dead ends’ for these bacteria, Legionella have nevertheless acquired molecular machinery to attack human cells via adaptation to their natural amoeba hosts. Our focus is on understanding how adaptation in the natural environment has primed Legionella to cross species barriers and infect humans. Through this work, we are excited to discover general principles for how bacteria and hosts drive each others’ evolution.