The Bailey lab studies the role genetic variation in immunity and disease from the perspective of both the host and pathogen.  Our work is primarily centered around malaria.   Key to these projects is how immunity shapes disease and how human and parasite variation interplay.
  • Do certain individuals have improved immune control of the parasite and disease?  
  • Are there certain pathogen variants that predispose to disease?  
  • What are the key parasite antigens targeted by an effective immune response and can such knowledge be leveraged to create an effective vaccine?  
  • How does falciparum malaria and EBV drive the etiology of the cancer Burkitt lymphoma?   
For all these questions we leverage high-throughput genomics and genetics and develop both experimental and computational tools to address these questions. Our work takes place in a large collaborative framework working with investigators across the world,

Malaria Genetics and Genomics

The main focus of our lab is malaria genomics within a large network of collaborators. Plasmodium falciparum and Plasmodium vivax are eukaryotic red cell parasites that still  causes signfiicant morbidity and mortality particularly in subSaharan Africa.   Our work traverses multiple fronts including:
  • basic genomics understanding the nature and pattern of genetic variation in the parasite
  • how host variation impacts disease and the parasite
  • understanding the immune response and parasite antigenic diversity  towards improving vaccines
  • the evolution  of antimalarial drug resistance to predict and control its development and spread
  • integrating genetic analyses into ecologic and immunologic models and frameworks

Burkitt lymphoma and Epstein Barr Virus

In malaria endemic regions Burkitt lymphoma is a major childhood cancer due to interactions of both Plasmodium falciparum malaria and Epstein Barr Virus. Our laboratory is interested in understanding tumor etiology and oncogenesisis. We are most interested in the role of variation in the infectious agents that may impact Burkitt lymphoma as well as tumor evolution and driver mutations. For this work we deploy a wide array of genomic tools in collaboration with virology and immunology collaborators. 

Other Projects

Type 1 Diabetes

We are working with collaborators to dissect the role of variation within the T cell receptors. Autoimmunity is a consequence of the infectious milieu over evolutionary time that leaves humans susceptibility. T cell receptor variation has not been closely studied despite its role as main interface with HLA proteins.


Babesia microti, a intracellular red cell parasite and distant relative of plasmodium,  is a major emerging pathogen  in the Northeast and Midwest transmitted by Ixodes ticks.  We have several project investigating genetic variation (extremely low) and optimizing methods of detection. 

Molecular blood typing

Antigenic variation on red cells is significant cause of blood incompatibility and hemolytic reactions as allogenic transfusions are recognized as nonself.  These differences have been driven in the past often by infectious agents such as malaria.    With Drs Lane and Westoff to develop high-throughput tools for clinical and epidemiological applications using  targeted next generation sequencing.