Many congratulations to Eleanor Silvester, winner of the 2017 Ker Memorial Prize

Very many congratulations to Eleanor Silvester from the School of Biological Sciences, winner of the 2017 Ker Memorial Prize in Infectious Diseases.

Eleanor (right) has been awarded the Ker Prize for the best PhD thesis submitted to the University of Edinburgh in 2016 for her work on quorum-sensing signals in African Trypanosomes, carried out in Keith Matthews' lab in the Institute of Immunology and Infection Research. 

As part of her prize Eleanor will present results from her thesis at the Edinburgh Infectious Diseases annual symposium on Thursday 1 June, in a talk entitled "Conservation of quorum-sensing signal responses and cross-species interactions between Trypanosoma brucei and Trypanosoma congolense". 

Eleanor's PhD research was supported by a studentship from the Biotechnology and Biological Sciences Research Council.

The Ker Prize is very generously supported by Miss Aileen Ker, in memory of two outstanding Edinburgh physicians, her grandfather Dr. Claude Buchanan Ker, and his son (her father), Dr. Frank Leighton Ker.  The glowing and heartfelt obituaries written for both these men, show the enormous regard and affection in which they were held, and to which the Ker Memorial Prize and Lecture now provide fitting testimony. 

The Ker family also support the presentation of the Ker Memorial Lecture, given by an eminent invited scientist in Infectious Diseases, which this year will be presented by Prof Peter Openshaw from Imperial Collge London.

About Eleanor

Eleanor’s bachelor’s degree was in Natural Sciences at the University of Cambridge, where she specialised in infectious diseases during her final year.  It was during the final year of her degree that she had her first experience of parasitology research, in the laboratory of Professor David Dunne investigating the developmental expression of an allergen-like protein produced by Schistosoma mansoni.

After working for a short time as a research assistant in a histopathology CRO in Cambridge, Eleanor moved to Edinburgh in 2012 to start a PhD in the Matthews lab. Her PhD explored whether quorum-sensing signal responses were conserved in different species of African trypanosomes and whether there was a potential for inter-specific cell-cell communication in co-infections.

Eleanor is currently continuing with her research in a postdoctoral position with Keith. 

Eleanor writing about her work

Animal African Trypanosomiasis is a disease affecting livestock in Africa that limits productivity and economic development. The disease is caused by single-celled parasites of the species Trypanosoma brucei brucei, Trypanosoma congolense or Trypanosoma vivax. These African trypanosomes replicate within the bloodstream of the mammalian host, and are transmitted between hosts by the blood-feeding tsetse fly. Frequently the parasites also coinfect the same host.

To ensure its continued survival a parasite population must not overwhelm its host before it can be transmitted. T. brucei has developed a density-sensing mechanism to facilitate this. The parasite population is maintained by proliferation of slender forms and these forms release a density-sensing signal known as SIF (stumpy induction factor). At high parasite density, SIF accumulates to a level that induces slender forms to develop into stumpy forms. Stumpy forms are growth arrested and so limit parasite numbers, prolonging host survival. They have features that allow them to continue development when taken up by feeding tsetse flies, enabling transmission.

T. congolense does not have slender and stumpy forms but, like T. brucei, must survive long enough in the host for transmission to occur. The aim of my thesis work was to establish whether these parasites control their growth through a density-sensing mechanism comparable to T. brucei, and if so whether the different trypanosome species could respond to each other’s signals when in mixed infections.

In T. congolense infections high parasite numbers were associated with a degree of growth arrest. Moreover, the T. congolense genome contained genes similar to those used in T. brucei for the SIF response, and one was able to compensate for the absence of a SIF-response gene in T. brucei, indicating functional equivalence. Furthermore, T. brucei responded to signals from T. congolense in vitro and in vivo driving premature stumpy formation.

My results demonstrate inter-communication between these parasite species, which has the potential to alter their virulence and transmission in co-infections.

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