Patterns in Age-Seroprevalence Consistent with Acquired Immunity against Trypanosoma brucei in Serengeti Lions
Susan C. Welburna b✉, Kim Picozzib, Paul G. Colemanc d, Craig Packere
- aCentre for Infectious Disease, College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, United Kingdom. sue.welburn@ed.ac.uk
- bCentre for Infectious Disease, College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh, United Kingdom
- cDepartment of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom
- dDepartment of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London, United Kingdom
- eDepartment of Ecology, Evolution, and Behavior, University of Minnesota, Minnesota, United States of America
- ✉Corresponding author
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Abstract
Trypanosomes cause disease in humans and livestock throughout sub-Saharan Africa. Although various species show evidence of clinical tolerance to trypanosomes, until now there has been no evidence of acquired immunity to natural infections. We discovered a distinct peak and decrease in age prevalence of T. brucei s.l. infection in wild African lions that is consistent with being driven by an exposure-dependent increase in cross-immunity following infections with the more genetically diverse species, T. congolense sensu latu. The causative agent of human sleeping sickness, T. brucei rhodesiense, disappears by 6 years of age apparently in response to cross-immunity from other trypanosomes, including the non-pathogenic subspecies, T. brucei brucei. These findings may suggest novel pathways for vaccinations against trypanosomiasis despite the notoriously complex antigenic surface proteins in these parasites.