ABSTRACT
BACKGROUND AND AIM: Trypanosomiasis, also known as surra, is an infectious disease with a wide host spectrum. In Indonesia, this disease is caused by Trypanosoma evansi. Various trypanocidal drugs have been used to treat this pathogen and subsequent disease. Yet, the long-term trypanocidal administration generates drug-resistant T. evansi. Some have identified genetic alterations in T. evansi transporter protein-coding genes that may be responsible for drug resistance. The Multidrug Resistance Protein E (MRPE) gene is a likely candidate gene responsible for the individual resistance. To date, no research has focused on T. evansi MRPE (TevMRPE) in this context. Hence, this research aimed at analyzing and characterizing the TevMRPE gene and protein using a bioinformatics approach. MATERIALS AND METHODS: T. evansi was isolated from buffalo suffering from surra in Ngawi Regency, Indonesia. Isolated T. evansi was inoculated and cultured in male mice. The T. evansi genome was isolated from mouse blood with a parasitemia degree as high as 105. A polymerase chain reaction procedure was conducted to amplify the putative MRPE coding gene. The amplicon was sequenced and analyzed using MEGA X, BLAST, and I-tasser softwares. RESULTS: The putative TevMRPE coding gene showed sequence similarity as high as 99.79% against the MRPE gene from Trypanosoma brucei gambiense. The protein profile and characteristics depicted that the putative TevMRPE protein was related to a family of Adenosine Triphosphate-Binding Cassette (ABC) transporter proteins. This family of transporter proteins plays a crucial role in the resistance toward several medicines. CONCLUSION: The obtained gene sequence in this research was identified as the TevMRPE. This gene is homologous to the T. brucei gambiense MRPE gene and possesses ligand active sites for Adenylyl Imidodiphosphate. In addition, MRPE contains enzyme active sites similar to the cystic fibrosis transmembrane conductance regulator. These data suggest that ABC transport proteins, like MRPE, may be necessary to confer trypanocidal drug resistance in T. evansi.
