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1. Molecular characterization and mapping of glucose-6-phosphate dehydrogenase (G6PD) mutations in the Greater Mekong Subregion

Author

Bancone, G, Menard, D, Khim, N, Kim, S, Canier, L, Nguong, C, Phommasone, K, Mayxay, M, Dittrich, S, Vongsouvath, M, Fievet, N, Le Hesran, J-Y, Briand, V, Keomany, S, Newton, PN, Gorsawun, G, Tardy, K, Chu, CS, Rattanapalroj, O, Dong, LT, Quang, HH, Tam-Uyen, N, Thuy-Nhien, N, Hien, TT, Kalnoky, M, Nosten, F, Shoklo Malaria Research Unit [Mae Sot, Thailand] (SMRU), Mahidol Oxford Tropical Medicine Research Unit (MORU), University of Oxford-Mahidol University [Bangkok]-Wellcome Trust-University of Oxford-Mahidol University [Bangkok]-Wellcome Trust, Centre for Tropical Medicine and Global Health [Oxford, UK], Nuffield Department of Medicine [Oxford, UK] (Big Data Institute), University of Oxford-University of Oxford, Institut Pasteur du Cambodge, Réseau International des Instituts Pasteur (RIIP), Biologie des Interactions Hôte-Parasite - Biology of Host-Parasite Interactions, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), National Center for Parasitology, Entomology and Malaria Control [Phnom Penh, Cambodia] (CNM), Lao-Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Mahidol University [Bangkok]-Mahosot Hospital, Institute of Research and Education Development [Vientiane, Lao People’s Democratic Republic], University of Health Sciences [Vientiane, Laos] (UHS), Foundation for Innovative New Diagnostics (FIND), Mère et enfant en milieu tropical : pathogènes, système de santé et transition épidémiologique (MERIT - UMR_D 216), Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5), Bordeaux population health (BPH), Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM), Salavan Provincial Hospital, Bureau of Vector Born Diseases [Bangkok, Thailande], Institute of Malariology, Parasitology, and Entomology [Ho Chi Minh City, Vietnam] (IMPE), Institute of Malariology, Parasitology, and Entomology [Quy Nhon, Vietnam] (IMPE), Hospital for Tropical Diseases - HTD [Ho Chi Minh City, Vietnam], Oxford University Clinical Research Unit [Ho Chi Minh City] (OUCRU), Diagnostics Program [Seattle, WA, USA] (PATH), Institut Pasteur [Paris], Communautés d’universités et établissements Sorbonne Paris Cité (COMUE Sorbonne Paris Cité), Université Sorbonne Paris Cité (USPC)-Chimie ParisTech-Paris Sciences et Lettres (PSL), Santé de la mère et de l'enfant en milieu tropical : épidémiologie génétique et périnatale, Université Paris Descartes - Paris 5 (UPD5), Ecosystèmes, biodiversité, évolution [Rennes] (ECOBIO), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut Ecologie et Environnement (INEE), Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Observatoire des Sciences de l'Univers de Rennes (OSUR)-Centre National de la Recherche Scientifique (CNRS), National Institute of Malariology, Parasitology and Entomology, Shoklo Malaria Research Unit [Mae Sot, Thailand] (Faculty of Tropical Medicine), Mahidol University [Bangkok]-Mahidol Oxford Tropical Medicine Research Unit (MORU), University of Oxford [Oxford]-Mahidol University [Bangkok]-Wellcome Trust-University of Oxford [Oxford]-Wellcome Trust, Wellcome Trust-Mahidol University [Bangkok]-University of Oxford [Oxford]-Wellcome Trust-Mahidol University [Bangkok]-University of Oxford [Oxford], University of Oxford [Oxford]-University of Oxford [Oxford], Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and Menard, Didier

Subjects
Adult, Male, lcsh:Arctic medicine. Tropical medicine, Adolescent, Genotype, lcsh:RC955-962, Research, Infant, Newborn, Genetic Variation, Infant, Glucosephosphate Dehydrogenase, Middle Aged, lcsh:Infectious and parasitic diseases, Young Adult, Glucosephosphate Dehydrogenase Deficiency, Child, Preschool, parasitic diseases, Prevalence, Humans, [SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, lcsh:RC109-216, Female, Child, [SDV.MP.PAR] Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, Asia, Southeastern
Abstract

Background Plasmodium vivax malaria elimination can only be achieved by the deployment of 8-aminoquinolines (primaquine and tafenoquine) in combination with ACT to kill both blood and liver-stage parasites. However, primaquine and the other 8-aminoquinolines cause dose-dependent haemolysis in subjects with G6PD deficiency, an X-linked disorder of red blood cells that is very common in populations living in tropical and subtropical areas. In order to inform safer use of 8-aminoquinolines in the Greater Mekong Subregion, a multi-centre study was carried out to assess the prevalence of G6PD deficiency and to identify the main G6PD variants in samples collected in Cambodia, Lao PDR, Myanmar, Thailand and Vietnam. Methods Blood samples were collected in the five countries during National Malaria Surveys or during Population Surveys. During Population Surveys samples were characterized for G6PD phenotype using the Fluorescent Spot Test. Samples were then genotyped for a panel of G6PD mutations. Results G6PD deficiency was found to be common in the region with an overall mean prevalence of deficient or mutated hemizygous males of 14.0%, ranging from a mean 7.3% in Thailand, 8.1% in Lao PDR, 8.9% in Vietnam, 15.8% in Myanmar and 18.8% in Cambodia. Mahidol and Viangchan mutations were the most common and widespread variants found among the nine investigated. Conclusions Owing to the high prevalence of G6PD deficiency in the Greater Mekong Subregion, strategies for vivax malaria elimination should include point-of-care G6PD testing (both qualitative and quantitative) to allow safe and wide treatment with 8-aminoquinolines. Electronic supplementary material The online version of this article (10.1186/s12936-019-2652-y) contains supplementary material, which is available to authorized users.

Published
2019
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2. Deciphering the genetic control of gene expression following Mycobacterium leprae antigen stimulation

Author

Guillaume Laval, Luis B. Barreiro, Yohann Nédélec, Erwin Schurr, Jeremy Manry, Vu Hong Thai, Vinicius M. Fava, Nguyen Van Thuc, Aurélie Cobat, Marianna Orlova, McGill University = Université McGill [Montréal, Canada], CHU Sainte Justine [Montréal], CRSN/Faculté de médecine Université de Montréal, Génétique Humaine des Maladies Infectieuses (Inserm U980), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Hospital for Tropical Diseases - HTD [Ho Chi Minh City, Vietnam], Génétique Evolutive Humaine - Human Evolutionary Genetics, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Centre de Bioinformatique, Biostatistique et Biologie Intégrative (C3BI), Université de Montréal (UdeM), This work was supported by a Foundation grant from the Canadian Institutes of Health Research (CIHR FDN – 14332) to ES. This research was supported through resource allocation in the Guillimin high performance computing cluster by Compute Canada (www.computecanada.ca) and Calcul Québec (http://www.calculquebec.ca/) (jrt-675-01). JM was supported by a CIHR fellowship (MFE-127384) and in part by a grant from the Laboratory of Excellence Integrative Biology of Emerging Infectious Diseases (LabEx IBEID: http://www.pasteur.fr/labex/ibeid), We thank all leprosy patients who participated in this study. We thank the members of the Schurr lab and the members of the laboratory for Human Genetics of Infectious Diseases in Paris for useful discussions and suggestions on this work. We thank the members of the Human Evolutionary Genetics laboratory, Institut Pasteur, Paris, and especially Maxime Rotival for useful discussions and suggestions on this work., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), Bidault, Floran, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, and Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, Bacterial Diseases, Cancer Research, Genome-wide association study, Genome-wide association studies, MESH: Down-Regulation, 0302 clinical medicine, Human genetics, Gene expression, Medicine and Health Sciences, MESH: Up-Regulation, Pathogen, Mycobacterium leprae, Genetics of disease, Genetics (clinical), MESH: Genetic Association Studies, Genetics, Principal Component Analysis, MESH: Polymorphism, Single Nucleotide, MESH: Genetic Predisposition to Disease, Genomics, 3. Good health, Up-Regulation, Actinobacteria, RNA, Bacterial, Infectious Diseases, Host-Pathogen Interactions, Gene ontologies, [SDV.IMM]Life Sciences [q-bio]/Immunology, Leprosy, MESH: RNA, Bacterial, Research Article, Neglected Tropical Diseases, lcsh:QH426-470, [SDV.IMM] Life Sciences [q-bio]/Immunology, Quantitative Trait Loci, Immunology, Down-Regulation, [SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics, Biology, Polymorphism, Single Nucleotide, 03 medical and health sciences, Immune system, medicine, Humans, Genetic Predisposition to Disease, Immune response, Molecular Biology, Gene, Ecology, Evolution, Behavior and Systematics, Genetic Association Studies, MESH: Principal Component Analysis, Antigens, Bacterial, MESH: Humans, Bacteria, MESH: Host-Pathogen Interactions, Organisms, Biology and Life Sciences, Computational Biology, medicine.disease, biology.organism_classification, Tropical Diseases, Genome Analysis, MESH: Quantitative Trait Loci, MESH: Leprosy, lcsh:Genetics, 030104 developmental biology, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Expression quantitative trait loci, MESH: Mycobacterium leprae, 030217 neurology & neurosurgery, MESH: Antigens, Bacterial
Abstract

Leprosy is a human infectious disease caused by Mycobacterium leprae. A strong host genetic contribution to leprosy susceptibility is well established. However, the modulation of the transcriptional response to infection and the mechanism(s) of disease control are poorly understood. To address this gap in knowledge of leprosy pathogenicity, we conducted a genome-wide search for expression quantitative trait loci (eQTL) that are associated with transcript variation before and after stimulation with M. leprae sonicate in whole blood cells. We show that M. leprae antigen stimulation mainly triggered the upregulation of immune related genes and that a substantial proportion of the differential gene expression is genetically controlled. Indeed, using stringent criteria, we identified 318 genes displaying cis-eQTL at an FDR of 0.01, including 66 genes displaying response-eQTL (reQTL), i.e. cis-eQTL that showed significant evidence for interaction with the M. leprae stimulus. Such reQTL correspond to regulatory variations that affect the interaction between human whole blood cells and M. leprae sonicate and, thus, likely between the human host and M. leprae bacilli. We found that reQTL were significantly enriched among binding sites of transcription factors that are activated in response to infection, and that they were enriched among single nucleotide polymorphisms (SNPs) associated with susceptibility to leprosy per se and Type-I Reaction, and seven of them have been targeted by recent positive selection. Our study suggested that natural selection shaped our genomic diversity to face pathogen exposure including M. leprae infection., Author summary Each year, 200,000 new leprosy cases are reported worldwide. While there is unambiguous evidence for a role of host genetics in leprosy pathogenesis, the mechanisms by which the human host fights the infection are poorly understood. Here, we highlight the search for naturally occurring genetic variations that modulate gene expression levels following exposure to sonicate of Mycobacterium leprae, the bacterium causing the disease. Because M. leprae is not cultivable and the genuine immune cells involved in the host response during infection are still unknown, we performed a genome-wide search for such genetic variations after stimulation of whole-blood from leprosy patients with M. leprae sonicate. This design allowed to provide a general framework for the genetic control of host responses to M. leprae and outlined the contribution of host genetics to leprosy pathogenesis. Among the M. leprae-dependent genetic regulators of gene expression levels there was an enrichment of variants (i) associated with leprosy, (ii) located in transcription factor binding sites and (iii) targeted by recent positive selection.

Published
2017
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