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Review

In silico prediction of protein–protein interaction between Glossina m. morsitans (Westwood, 1851) and Trypanosoma brucei (Kinetoplastida: Trypanosomatidae)

Eunice Muriithi

Received:

22 Aug 2017

Accepted:

30 May 2018

Published:

14 Jun 2018

Volume:

11

Issue:

1

Keywords:

Trypanosoma brucei, Glossina m. morsitans, protein–protein interaction, Trypanosomiasis

Abstract:

Trypanosoma brucei is a pathogenic protozoa that causes chronic Human African Trypanosomiasis and African Animal Trypanosomiasis. The pathogenic parasite is transmitted to humans by the tsetse fly, Glossina m. morsitans. Trypanosomiasis control strategies have targeted either the tsetse vector or the parasite. Most of the biological processes in a living cell are controlled by protein–protein interactions (PPI). Prediction of vector host–parasite protein interactions could give an insight into the mechanism of blocking transmission through parasite interference and identify potential vaccine targets. Prediction of protein interactions and orthologous relatedness was done between Glossina m. morsitans (the vector host) and T. brucei (the parasite) using information on conserved orthologous protein interactions in other organisms (interologs). Orthologues from both species were identified using a Markov cluster algorithm of the OrthoMCL software. The Host-Pathogen Interaction Database (HPIDB) and BIANA Interolog Prediction server (BIPS) identified interologs in Glossina m. morsitans and T. brucei. Among the predicted proteins from BIPS were T. brucei tubulin alpha chain, tubulin beta chain, dynein light chain-putative and calmodulin, which were observed to act as hubs connecting to Glossina’s Ubiquitin-40S ribosomal protein S27a fusion protein, dyenin light chain type 1, heat shock protein cognate 3, Gamma-aminobutyric acid receptor-associated protein, putative glycerate kinase and Ribosomal protein S14b. These proteins are implicated in the cellular transportation mechanism of both the vector and the parasite as well as the host defense mechanism. Those predicted from HPIBD were Glossina s-adenosylmethionine synthetase, DNA helicase, ubiquitin protein ligase, AAA+-type ATPase, Rab protein 6, WD40 repeat-containing protein and serine/threonine protein phosphatase, observed to act as hubs connecting to parasitic s-adenosylmethionine synthetase, elongation factor 1-alpha 2, Histone H2A, katanin, lipoic acid synthetase, PolyUbiquitin and serine/threonine protein kinase. This study gives an important insight into the PPI involved in Glossina–Trypanosoma associations that may be involved in the immune response of Glossina m. morsitans and evasion by T. brucei. Some of the interactions may help in the trypanosome’s transformation within the vector host. These observations will give a better understanding of parasite transmission biology and may advance efforts towards transmission-blocking vaccines.

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