Data from: Whole genome sequencing shows sleeping sickness relapse is due to parasite regrowth and not reinfection
Data files
Oct 08, 2015 version files 27 GB
-
141BT_R1.zip
704.80 MB
-
141BT_R2.zip
709.35 MB
-
146AT_R1.zip
833.95 MB
-
146AT_R2.zip
841.84 MB
-
146BT_R1.zip
770.69 MB
-
146BT_R2.zip
776.48 MB
-
148AT_R1.zip
918.16 MB
-
148AT_R2.zip
926.04 MB
-
148BT_R1.zip
680.49 MB
-
148BT_R2.zip
686 MB
-
15RE_R1.zip
665.37 MB
-
15RE_R2.zip
672.47 MB
-
163AT_R1.zip
341.85 MB
-
163AT_R2.zip
345.63 MB
-
163REL_R1.zip
866.80 MB
-
163REL_R2.zip
877.53 MB
-
340AT_R1.zip
674.84 MB
-
340AT_R2.zip
681.85 MB
-
346AT_R1.zip
821.05 MB
-
346AT_R2.zip
828.08 MB
-
346BT_R1.zip
707.22 MB
-
346BT_R2.zip
712.73 MB
-
346REL_R1.zip
600.95 MB
-
346REL_R2.zip
605.13 MB
-
348BT_R1.zip
676.46 MB
-
348BT_R2.zip
680.99 MB
-
349AT_R1.zip
664.40 MB
-
349AT_R2.zip
669.17 MB
-
349BT_R1.zip
737.85 MB
-
349BT_R2.zip
743.76 MB
-
378BT_R1.zip
733.15 MB
-
378BT_R2.zip
740.99 MB
-
45BT_R1.zip
768.97 MB
-
45BT_R2.zip
778.33 MB
-
57AT_R1.zip
796.98 MB
-
57AT_R2.zip
805.77 MB
-
85BT_R1.zip
472.88 MB
-
85BT_R2.zip
478.19 MB
Abstract
The trypanosome Trypanosoma brucei gambiense (Tbg) is a cause of human African trypanosomiasis (HAT) endemic to many parts of sub-Saharan Africa. The disease is almost invariably fatal if untreated and there is no vaccine, which makes monitoring and managing drug resistance highly relevant. A recent study of HAT cases from the Democratic Republic of the Congo reported a high incidence of relapses in patients treated with melarsoprol. Of the 19 Tbg strains isolated from patients enrolled in this study, four pairs were obtained from the same patient before treatment and after relapse. We used whole genome sequencing to investigate whether these patients were infected with a new strain, or if the original strain had regrown to pathogenic levels. Clustering analysis of 5938 single nucleotide polymorphisms supports the hypothesis of regrowth of the original strain, as we found that strains isolated before and after treatment from the same patient were more similar to each other than to other isolates. We also identified 23 novel genes that could affect melarsoprol sensitivity, representing a promising new set of targets for future functional studies. This work exemplifies the utility of using evolutionary approaches to provide novel insights and tools for disease control.
