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.
Highlights
Trypanosomes transmitted by tsetse flies are a major constraint to the health and economic development of many of the poorest regions of Africa
Serengeti lions show an asymptotic age prevalence of the non-pathogenic Trypanosoma congolense in contrast to a strong peak and decrease in age prevalence of the pathogenic T. brucei s.l. This pattern suggests that lions may gain cross-immunity to T. brucei from repeated exposure to the more genetically diverse T. congolense
Lions may gain more effective cross immunity than other host species owing to their frequent consumption of infected prey animals, these findings suggest possible strategies for designing effective vaccines against sleeping sickness in livestock and humans
Summary
The search for effective vaccines to protect both humans and their livestock populations from the trypanosomiases has proved to be one of the greatest and most elusive challenges in global public health [1]. This is because of the unique mechanism of immune invasion employed by the trypanosomes. Persistence of trypanosome infection depends on evasion of the host immune response through a complex system of antigenic variation of the variant surface glycoprotein (VSG) that shields the cell [2]. The absence of any natural examples of immunity to trypanosomes has been a major constraint to vaccine development
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