Active Infection & Immunity Genetics & Molecular Biology

Emergence and transmission of Trypanosoma brucei rhodesiense and the Serum Resistance Associated gene in wildlife hosts

In plain English

AI plain-English summary

A single gene separates a harmless livestock parasite from one that causes a fatal human disease, and this project will track how that gene moves through wild animals in Africa. Human African Trypanosomiasis, or sleeping sickness, kills thousands of people each year when tsetse flies transmit the parasite *Trypanosoma brucei rhodesiense*. The parasite is genetically identical to a livestock-infecting form except for one gene—the Serum Resistance Associated (SRA) gene—that makes it able to infect humans. Researchers have not been able to study how this gene spreads in wildlife because collecting tissue samples from wild animals is extremely difficult. This project will validate a non-invasive method: detecting the parasite in animal faeces. The researcher will collect faecal samples from multiple wildlife species, then sequence the parasites' genomes to map how SRA emerges and moves between animal hosts. If successful, this work will reveal why human sleeping sickness cases sometimes spike suddenly, turning into epidemics. Understanding the wildlife reservoir could allow health authorities to predict outbreaks before they reach people, and to target tsetse control efforts more precisely. The research is fundamentally about parasite evolution and transmission ecology, not about developing a new drug or vaccine—but knowing how the SRA gene circulates is a necessary step toward any future intervention that might block it.

View original technical description
Human African Trypanosomiasis (HAT, or African Sleeping Sickness) is caused by the parasite Trypanosoma brucei and vectored by tsetse flies. T. brucei rhodesiense (Tbr) causes the acute form of human disease, and morphologically identical T. brucei brucei (Tbb) infects livestock but not humans. There is a single gene difference between Tbb and Tbr, the Serum Resistance Associated (SRA) gene, which causes human infectivity. Recombination between Tbb and Tbr can occur, but there is limited understanding of how these parasites circulate in the wildlife reservoir. Wildlife samples are challenging to obtain, and this has limited previous investigations of HAT in wildlife. T. brucei was found to be detectable in cattle faeces, therefore faecal sampling is a possible way to increase sample size. My project aims to investigate the epidemiology of Tbb and Tbr in wildlife populations, identifying how human infective parasites emerge and spread. I will validate faecal sampling in wildlife and collect samples from a range of wildlife species, to investigate the impact of host factors on parasite prevalence. This will be followed by sequencing and phylogenetic analysis to investigate parasite population structures. Overall, this will provide insight what causes sudden increases in human cases of HAT, leading to epidemics.

View the original record at the funder ↗

Researchers

Abigail Carruthers (EPMC Awardee)

Related Research

Grants with similar aims, by meaning.

Understanding host-parasite interactions of Trypanosoma parasites in skin colonisation of their mammalian hosts
Characterisation of uptake and sub-cellular transit of human serum trypanolytic factors by Trypanosoma brucei
High throughput decoding of virulence mechanisms in African trypanosomes.
Expression profiling of African trypanosomes in human and primate hosts: Identification of biomarkers for diagnosis, drug target identification and dissection of virulence pathways.
Genomic analysis of the impact of sexual recombination on the segregation of virulence genes in African trypanosomes

Original classification

PhD Studentship (Basic)

Plain English summaries and category classifications on this site are generated by AI and may not perfectly reflect the original research.