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Sent on Tuesday, 2011 Nov 01Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Nucleic Acids Res. 2011 Oct 27. [Epub ahead of print]Crystal structure of a heterodimer of editosome interaction proteins in complex with two copies of a cross-reacting nanobody.Park YJ, Pardon E, Wu M, Steyaert J, Hol WG.SourceDepartment of Biochemistry, Biomolecular Structure Center, School of Medicine, University of Washington, PO Box 357742, Seattle WA 98195, USA, Structural Biology Brussels, Vrije Universiteit Brussel, and Department of Structural Biology, VIB, Vrije Universiteit Brussel, B-1050, Brussel. AbstractThe parasite Trypanosoma brucei, the causative agent of sleeping sickness across sub-Saharan Africa, depends on a remarkable U-insertion/deletion RNA editing process in its mitochondrion. A approximately 20 S multi-protein complex, called the editosome, is an essential machinery for editing pre-mRNA molecules encoding the majority of mitochondrial proteins. Editosomes contain a common core of twelve proteins where six OB-fold interaction proteins, called A1-A6, play a crucial role. Here, we report the structure of two single-strand nucleic acid-binding OB-folds from interaction proteins A3 and A6 that surprisingly, form a heterodimer. Crystal growth required the assistance of an anti-A3 nanobody as a crystallization chaperone. Unexpectedly, this anti-A3 nanobody binds to both A3(OB) and A6, despite only ∼40% amino acid sequence identity between the OB-folds of A3 and A6. The A3(OB)-A6 heterodimer buries 35% more surface area than the A6 homodimer. This is attributed mainly to the presence of a conserved Pro-rich loop in A3(OB). The implications of the A3(OB)-A6 heterodimer, and of a dimer of heterodimers observed in the crystals, for the architecture of the editosome are profound, resulting in a proposal of a 'five OB-fold center' in the core of the editosome. |
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| 2. | Genome Res. 2011 Oct 28. [Epub ahead of print]Chromosome and gene copy number variation allow major structural change between species and strains of Leishmania.Rogers MB, Hilley JD, Dickens NJ, Wilkes J, Bates PA, Depledge DP, Harris D, Her Y, Herzyk P, Imamura H, Otto TD, Sanders M, Seeger K, Dujardin JC, Berriman M, Smith DF, Hertz-Fowler C, Mottram JC.SourceWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge CB10 1SA, United Kingdom; AbstractLeishmania parasites cause a spectrum of clinical pathology in humans ranging from disfiguring cutaneous lesions to fatal visceral leishmaniasis. We have generated a reference genome for Leishmania mexicana and refined the reference genomes for Leishmania major, Leishmania infantum, and Leishmania braziliensis. This has allowed the identification of a remarkably low number of genes or paralog groups (2, 14, 19, and 67, respectively) unique to one species. These were found to be conserved in additional isolates of the same species. We have predicted allelic variation and find that in these isolates, L. major and L. infantum have a surprisingly low number of predicted heterozygous SNPs compared with L. braziliensis and L. mexicana. We used short read coverage to infer ploidy and gene copy numbers, identifying large copy number variations between species, with 200 tandem gene arrays in L. major and 132 in L. mexicana. Chromosome copy number also varied significantly between species, with nine supernumerary chromosomes in L. infantum, four in L. mexicana, two in L. braziliensis, and one in L. major. A significant bias against gene arrays on supernumerary chromosomes was shown to exist, indicating that duplication events occur more frequently on disomic chromosomes. Taken together, our data demonstrate that there is little variation in unique gene content across Leishmania species, but large-scale genetic heterogeneity can result through gene amplification on disomic chromosomes and variation in chromosome number. Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression in response to environmental conditions in the host, providing a genetic basis for disease tropism. |
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| 3. | Genome Res. 2011 Oct 28. [Epub ahead of print]Whole genome sequencing of multiple Leishmania donovani clinical isolates provides insights into population structure and mechanisms of drug resistance.Downing T, Imamura H, Decuypere S, Clark TG, Coombs GH, Cotton JA, Hilley JD, de Doncker S, Maes I, Mottram JC, Quail MA, Rijal S, Sanders M, Schönian G, Stark O, Sundar S, Vanaerschot M, Hertz-Fowler C, Dujardin JC, Berriman M.SourceWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, United Kingdom; AbstractVisceral leishmaniasis is a potentially fatal disease endemic to large parts of Asia and Africa, primarily caused by the protozoan parasite Leishmania donovani. Here, we report a high-quality reference genome sequence for a strain of L. donovani from Nepal, and use this sequence to study variation in a set of 16 related clinical lines, isolated from visceral leishmaniasis patients from the same region, which also differ in their response to in vitro drug susceptibility. We show that whole-genome sequence data reveals genetic structure within these lines not shown by multilocus typing, and suggests that drug resistance has emerged multiple times in this closely related set of lines. Sequence comparisons with other Leishmania species and analysis of single-nucleotide diversity within our sample showed evidence of selection acting in a range of surface- and transport-related genes, including genes associated with drug resistance. Against a background of relative genetic homogeneity, we found extensive variation in chromosome copy number between our lines. Other forms of structural variation were significantly associated with drug resistance, notably including gene dosage and the copy number of an experimentally verified circular episome present in all lines and described here for the first time. This study provides a basis for more powerful molecular profiling of visceral leishmaniasis, providing additional power to track the drug resistance and epidemiology of an important human pathogen. |
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| 4. | Parasitol Res. 2011 Oct 25. [Epub ahead of print]In vitro antileishmanial and antitrypanosomal activities of five medicinal plants from Burkina Faso.Sawadogo WR, Le Douaron G, Maciuk A, Bories C, Loiseau PM, Figadère B, Guissou IP, Nacoulma OG.SourceInstitut de Recherche en Sciences de la Santé (IRSS/CNRST), 03 BP 7192, Ouagadougou 03, Burkina Faso, richardsawadogo@hotmail.com. AbstractAfter ethnobotanical surveys in central and western regions of Burkina Faso, five plants namely Lantana ukambensis (Verbenaceae), Xeoderris sthulmannii (Fabaceae), Parinari curatellifollia (Chrysobalanaceae), Ozoroa insignis (Anacardiaceae), and Ficus platyphylla (Moraceae) were selected for their traditional use in the treatment of parasitic diseases and cancer. Our previous studies have focused on the phytochemical, genotoxicity, antioxidant, and antiproliferative activities of these plants. In this study, the methanol extract of each plant was tested to reveal probable antileishmanial and antitrypanosomal activities. Colorimetric and spectrophotometric methods were used for the detection of antileishmanial and antitrypanosomal activities. Leishmania donovani (LV9 WT) and Trypanosoma brucei brucei GVR 35 were used to test the antileishmanial and antitrypanosomal activities, respectively. All extracts of tested plants showed a significant antitrypanosomal activity with minimum lethal concentrations between 1.5 and 25 μg/ml, the L. ukambensis extract being the most active. In the antileishmanial test, only the extract from L. ukambensis showed significant activity with an inhibitory concentration (IC(50)) of 6.9 μg/ml. The results of this study contribute to the promotion of traditional medicine products and are preliminary for the isolation of new natural molecules for the treatment of leishmaniasis and trypanosomiasis. |
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| 5. | Infez Med. 2011 Sep 1;19(3):152-156.[Which screening for Leishmania infantum in asymptomatic blood donors?] [Article in Italian] Tordini G, Puttini C, Rossetti B, Sammarro G, Fanetti A, Cianchino S, Valoriani B, Fossombroni V, Campoccia G, Cavion MA, Zanelli G.SourceSezione Malattie Infettive Universitarie, Dipartimento Biotecnologie, Universita di Siena, Azienda Ospedaliera Universitaria Senese; U.O.C. Immunoematologia Trasfusionale, Dipartimento dei Servizi, Azienda Ospedaliera Universitaria Senese, Siena, Italy. AbstractLeishmaniasis is a protozoan infection endemic in Italy with a greatly underestimated prevalence. The recent documentation of parasitaemia in blood donors is a cause of concern for blood safety. Because there is no screening against leishmania, we performed a study to assess the presence of protozoa in blood donors of Siena district (Tuscany) during the seasonal activity of the vector. From June to October 2007, 162 patients were screened for Leishmania infantum by indirect immunofluorescence serology (IFAT) and PCR for kinetoplast (kDNA). No subject was positive for antibodies, while 11 samples (6.8%) were positive for kDNA. A second PCR (nested-PCR) was negative for all kDNA positive individuals and other subjects for a total of 55 samples (33% of total subjects). The sequence analysis of three samples positive for kDNA was compatible with mitochondrial DNA. Through the techniques used, we were unable to confirm the presence of leishmania in the blood of the subjects studied. The choice of the diagnostic protocol in blood donors remains an open issue as molecular analysis (kDNA) seems to suggest, in our experience, limits of specificity. |
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| 6. | Clin Med. 2011 Oct;11(5):492-7.Leishmaniasis.Moore EM, Lockwood DN.SourceHospital for Tropical Diseases, University College London Hospital, London. AbstractLeishmaniasis is an uncommon infectious disease in the UK with a variety of clinical presentations. Physicians should remember to consider this diagnosis in patients with an appropriate travel history (including the Mediterranean basin) and seek help with diagnostics from a specialised parasitology laboratory. Treatment regimens may be unfamiliar to the general physician, and thus should also be discussed with an expert. |
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| 7. | Phytochemistry. 2011 Aug;72(11-12):1424-30. Epub 2011 May 11.Schistosomicidal and trypanocidal structure-activity relationships for (±)-licarin A and its (-)- and (+)-enantiomers.Pe reira AC, Magalhães LG, Gonçalves UO, Luz PP, Moraes AC, Rodrigues V, da Matta Guedes PM, da Silva Filho AA, Cunha WR, Bastos JK, Nanayakkara NP, e Silva ML.SourceGrupo de Pesquisas em Produtos Naturais, Núcleo de Ciências Exatas e Tecnológicas, Universidade de Franca, Avenida Dr. Armando Salles de Oliveira 2001, 14404-600 Franca, SP, Brazil. Abstract(±)-Licarin A (1) was obtained by oxidative coupling, and its enantiomers, (-)-licarin A (2) and (+)-licarin A (3), were resolved by chiral HPLC. Schistosomicidal and trypanocidal activities of these compounds were evaluated in vitro against Schistosoma mansoni adult worms and trypomastigote forms of Trypanosoma cruzi. The racemic mixture (1) displayed significant schistosomicidal activity with an LC₅₀ value of 53.57 μM and moderate trypanocidal activity with an IC₅₀ value of 127.17 μM. On the other hand, the (-)-enantiomer (2), displaying a LC₅₀ value of 91.71 μM, was more active against S. mansoni than the (+)-enantiomer (3), which did not show activity. For the trypanocidal assay, enantiomer 2 showed more significant activity (IC₅₀ of 23.46 μM) than enantiomer 3, which showed an IC₅₀ value of 87.73 μM. Therefore, these results suggest that (±)-licarin A (1) and (-)-licarin A (2) are promising compounds that could be used for the development of schistosomicidal and trypanocidal agents. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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