The vast majority of newly emerging infectious diseases can be traced back to wild animals. Of these zoonoses, viruses pose the greatest pandemic threat. The overall research goal of the Warren lab is to better understand how viruses adapt to infect new host species. We aim to use knowledge gained through the analysis of virus structure, function, and host interactions to identify fundamental biological processes that influence disease emergence.
The research projects in the Warren lab follow several lines of investigation that center around the study of the evolution and biology of virus host switching, and the molecular characterization of animal viruses with potential for zoonosis.
Virus-receptor interactions and their evolution. In order to initiate an infection, viruses must bind to specific receptor molecules on target cells. Most viruses are exquisitely fine-tuned to the receptors encoded by their natural host. Thus, subtle differences in receptor sequences that distinguish the old and new host may impose species barriers to virus host switching. The Warren lab seeks to define rules of virus-receptor engagement that predict which viruses have the potential to cross species barriers.
Intracellular factors dictate virus tropism and host switching potential. After a virus binds to its receptor, restriction of infection may also occur at multiple stages of the viral replication cycle within target cells. Most notably, host cellular factors induced by interferon (cellular immunity factors) act as barriers to virus host switching. Research in the Warren lab explores how viruses evolve to antagonize or evade cellular immunity factors.
Evaluating the zoonotic potential of novel viruses discovered in animals. Ambitious efforts are underway to sequence and catalog animal viromes—using genome sequencing tools and metagenomic analyses to identify animal viruses of high risk for zoonosis. My lab will establish experimental tools and pipelines to broadly study animal viruses of potential zoonotic concern.