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Citations: 1319
H-Index: 18
i10-index: 28
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2017
Cuypers, Bart; den Broeck, Frederik Van; Reet, Nick Van; Meehan, Conor J; Cauchard, Julien; Wilkes, Jonathan M; Claes, Filip; Goddeeris, Bruno; Birhanu, Hadush; Dujardin, Jean-Claude; Laukens, Kris; Büscher, Philippe; Deborggraeve, Stijn
Genome-Wide SNP Analysis Reveals Distinct Origins of Trypanosoma evansi and Trypanosoma equiperdum Journal Article
In: Genome Biology and Evolution, vol. 9, no. 8, pp. 1990-1997, 2017, ISSN: 1759-6653.
@article{Cuypers2017b,
title = {Genome-Wide SNP Analysis Reveals Distinct Origins of Trypanosoma evansi and Trypanosoma equiperdum},
author = {Bart Cuypers and Frederik Van den Broeck and Nick Van Reet and Conor J Meehan and Julien Cauchard and Jonathan M Wilkes and Filip Claes and Bruno Goddeeris and Hadush Birhanu and Jean-Claude Dujardin and Kris Laukens and Philippe B\"{u}scher and Stijn Deborggraeve},
url = {https://doi.org/10.1093/gbe/evx102},
doi = {10.1093/gbe/evx102},
issn = {1759-6653},
year = {2017},
date = {2017-05-25},
journal = {Genome Biology and Evolution},
volume = {9},
number = {8},
pages = {1990-1997},
abstract = {Trypanosomes cause a variety of diseases in man and domestic animals in Africa, Latin America, and Asia. In the Trypanozoon subgenus, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense cause human African trypanosomiasis, whereas Trypanosoma brucei brucei, Trypanosoma evansi, and Trypanosoma equiperdum are responsible for nagana, surra, and dourine in domestic animals, respectively. The genetic relationships between T. evansi and T. equiperdum and other Trypanozoon species remain unclear because the majority of phylogenetic analyses has been based on only a few genes. In this study, we have conducted a phylogenetic analysis based on genome-wide SNP analysis comprising 56 genomes from the Trypanozoon subgenus. Our data reveal that T. equiperdum has emerged at least once in Eastern Africa and T. evansi at two independent occasions in Western Africa. The genomes within the T. equiperdum and T. evansi monophyletic clusters show extremely little variation, probably due to the clonal spread linked to the independence from tsetse flies for their transmission.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2016
Imamura, Hideo; Downing, Tim; den Broeck, Frederik Van; Sanders, Mandy J; Rijal, Suman; Sundar, Shyam; Mannaert, An; Vanaerschot, Manu; Berg, Maya; Muylder, Géraldine De; Dumetz, Franck; Cuypers, Bart; Maes, Ilse; Domagalska, Malgorzata; Decuypere, Saskia; Rai, Keshav; Uranw, Surendra; Bhattarai, Narayan Raj; Khanal, Basudha; Prajapati, Vijay Kumar; Sharma, Smriti; Stark, Olivia; Schönian, Gabriele; Koning, Harry P De; Settimo, Luca; Vanhollebeke, Benoit; Roy, Syamal; Ostyn, Bart; Boelaert, Marleen; Maes, Louis; Berriman, Matthew; Dujardin, Jean-Claude; Cotton, James A
Evolutionary genomics of epidemic visceral leishmaniasis in the Indian subcontinent Journal Article
In: eLife, vol. 5, pp. e12613, 2016, ISSN: 2050-084X.
@article{10.7554/eLife.12613,
title = {Evolutionary genomics of epidemic visceral leishmaniasis in the Indian subcontinent},
author = {Hideo Imamura and Tim Downing and Frederik Van den Broeck and Mandy J Sanders and Suman Rijal and Shyam Sundar and An Mannaert and Manu Vanaerschot and Maya Berg and G\'{e}raldine De Muylder and Franck Dumetz and Bart Cuypers and Ilse Maes and Malgorzata Domagalska and Saskia Decuypere and Keshav Rai and Surendra Uranw and Narayan Raj Bhattarai and Basudha Khanal and Vijay Kumar Prajapati and Smriti Sharma and Olivia Stark and Gabriele Sch\"{o}nian and Harry P De Koning and Luca Settimo and Benoit Vanhollebeke and Syamal Roy and Bart Ostyn and Marleen Boelaert and Louis Maes and Matthew Berriman and Jean-Claude Dujardin and James A Cotton},
editor = {Dominique Soldati-Favre},
url = {https://doi.org/10.7554/eLife.12613},
doi = {10.7554/eLife.12613},
issn = {2050-084X},
year = {2016},
date = {2016-03-01},
journal = {eLife},
volume = {5},
pages = {e12613},
publisher = {eLife Sciences Publications, Ltd},
abstract = {textitLeishmania donovani causes visceral leishmaniasis (VL), the second most deadly vector-borne parasitic disease. A recent epidemic in the Indian subcontinent (ISC) caused up to 80% of global VL and over 30,000 deaths per year. Resistance against antimonial drugs has probably been a contributing factor in the persistence of this epidemic. Here we use whole genome sequences from 204 clinical isolates to track the evolution and epidemiology of textitL. donovani from the ISC. We identify independent radiations that have emerged since a bottleneck coincident with 1960s DDT spraying campaigns. A genetically distinct population frequently resistant to antimonials has a two base-pair insertion in the aquaglyceroporin gene LdAQP1 that prevents the transport of trivalent antimonials. We find evidence of genetic exchange between ISC populations, and show that the mutation in LdAQP1 has spread by recombination. Our results reveal the complexity of textitL. donovani evolution in the ISC in response to drug treatment.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Cuypers, Bart; Lecordier, Laurence; Meehan, Conor J; den Broeck, Frederik Van; Imamura, Hideo; Büscher, Philippe; Dujardin, Jean-Claude; Laukens, Kris; Schnaufer, Achim; Dewar, Caroline; Lewis, Michael; Balmer, Oliver; Azurago, Thomas; Kyei-Faried, Sardick; Ohene, Sally-Ann; Duah, Boateng; Homiah, Prince; Mensah, Ebenezer Kofi; Anleah, Francis; Franco, Jose Ramon; Pays, Etienne; Deborggraeve, Stijn
Apolipoprotein L1 Variant Associated with Increased Susceptibility to Trypanosome Infection Journal Article
In: mBio, vol. 7, no. 2, 2016.
@article{Cuyperse02198-15,
title = {Apolipoprotein L1 Variant Associated with Increased Susceptibility to Trypanosome Infection},
author = {Bart Cuypers and Laurence Lecordier and Conor J Meehan and Frederik Van den Broeck and Hideo Imamura and Philippe B\"{u}scher and Jean-Claude Dujardin and Kris Laukens and Achim Schnaufer and Caroline Dewar and Michael Lewis and Oliver Balmer and Thomas Azurago and Sardick Kyei-Faried and Sally-Ann Ohene and Boateng Duah and Prince Homiah and Ebenezer Kofi Mensah and Francis Anleah and Jose Ramon Franco and Etienne Pays and Stijn Deborggraeve},
editor = {Michael P Barrett and John C Boothroyd},
url = {https://mbio.asm.org/content/7/2/e02198-15},
doi = {10.1128/mBio.02198-15},
year = {2016},
date = {2016-01-01},
journal = {mBio},
volume = {7},
number = {2},
publisher = {American Society for Microbiology},
abstract = {African trypanosomes, except Trypanosoma brucei gambiense and Trypanosoma~brucei~rhodesiense, which cause human African trypanosomiasis, are lysed by the human serum protein apolipoprotein L1 (ApoL1). These two subspecies can resist human ApoL1 because they express the serum resistance proteins T. b. gambiense glycoprotein (TgsGP) and serum resistance-associated protein (SRA), respectively. Whereas in T.~b.~rhodesiense, SRA is necessary and sufficient to inhibit ApoL1, in T.~b.~gambiense, TgsGP cannot protect against high ApoL1 uptake, so different additional mechanisms contribute to limit this uptake. Here we report a complex interplay between trypanosomes and an ApoL1 variant, revealing important insights into innate human immunity against these parasites. Using whole-genome sequencing, we characterized an atypical T.~b.~gambiense infection in a patient in Ghana. We show that the infecting trypanosome has diverged from the classical T.~b.~gambiense strains and lacks the TgsGP defense mechanism against human serum. By sequencing the ApoL1 gene of the patient and subsequent in vitro mutagenesis experiments, we demonstrate that a homozygous missense substitution (N264K) in the membrane-addressing domain of this ApoL1 variant knocks down the trypanolytic activity, allowing the trypanosome to avoid ApoL1-mediated immunity.IMPORTANCE Most African trypanosomes are lysed by the ApoL1 protein in human serum. Only the subspecies Trypanosoma b. gambiense and T.~b.~rhodesiense can resist lysis by ApoL1 because they express specific serum resistance proteins. We here report a complex interplay between trypanosomes and an ApoL1 variant characterized by a homozygous missense substitution (N264K) in the domain that we hypothesize interacts with the endolysosomal membranes of trypanosomes. The N264K substitution knocks down the lytic activity of ApoL1 against T.~b.~gambiense strains lacking the TgsGP defense mechanism and against T.~b.~rhodesiense if N264K is accompanied by additional substitutions in the SRA-interacting domain. Our data suggest that populations with high frequencies of the homozygous N264K ApoL1 variant may be at increased risk of contracting human African trypanosomiasis.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2015
Gryseels, Sophie; Rieger, Toni; Oestereich, Lisa; Cuypers, Bart; Borremans, Benny; Makundi, Rhodes; Leirs, Herwig; Günther, Stephan; de Bellocq], Joëlle [Goüy
In: Virology, vol. 476, pp. 249 - 256, 2015, ISSN: 0042-6822.
@article{GRYSEELS2015249,
title = {Gairo virus, a novel arenavirus of the widespread Mastomys natalensis: Genetically divergent, but ecologically similar to Lassa and Morogoro viruses},
author = {Sophie Gryseels and Toni Rieger and Lisa Oestereich and Bart Cuypers and Benny Borremans and Rhodes Makundi and Herwig Leirs and Stephan G\"{u}nther and Jo\"{e}lle [Go\"{u}y de Bellocq]},
url = {http://www.sciencedirect.com/science/article/pii/S0042682214005480},
doi = {https://doi.org/10.1016/j.virol.2014.12.011},
issn = {0042-6822},
year = {2015},
date = {2015-01-01},
journal = {Virology},
volume = {476},
pages = {249 - 256},
abstract = {Despite its near pan-African range, the Natal multimammate mouse, Mastomys natalensis, carries the human pathogen Lassa virus only in West Africa, while the seemingly non-pathogenic arenaviruses Mopeia, Morogoro, and Luna have been detected in this semi-commensal rodent in Mozambique/Zimbabwe, Tanzania and Zambia, respectively. Here, we describe a novel arenavirus in M. natalensis from Gairo district of central Tanzania, for which we propose the name “Gairo virus”. Surprisingly, the virus is not closely related with Morogoro virus that infects M. natalensis only 90km south of Gairo, but clusters phylogenetically with Mobala-like viruses that infect non-M. natalensis host species in Central African Republic and Ethiopia. Despite the evolutionary distance, Gairo virus shares basic ecological features with the other M. natalensis-borne viruses Lassa and Morogoro. Our data show that M. natalensis, carrying distantly related viruses even in the same geographical area, is a potent reservoir host for a variety of arenaviruses.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}