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Article ; Online: Human genetics of Buruli ulcer.

Manry, Jeremy

2020 Volume 139, Issue 6-7, Page(s) 847–853

Abstract: Buruli ulcer, the third most common mycobacterial disease worldwide, is caused by Mycobacterium ulcerans and characterized by devastating necrotizing skin lesions. Susceptibility to Buruli ulcer is thought to depend on host genetics, but very few genetic ...

Abstract	Buruli ulcer, the third most common mycobacterial disease worldwide, is caused by Mycobacterium ulcerans and characterized by devastating necrotizing skin lesions. Susceptibility to Buruli ulcer is thought to depend on host genetics, but very few genetic studies have been performed. The identification of a microdeletion on chromosome 8 in a familial form of severe Buruli ulcer suggested a monogenic basis of susceptibility. The role of common host genetic variants in Buruli ulcer development has been investigated in only three candidate-gene studies targeting genes involved in mycobacterial diseases. A recent genome-wide association study suggested a probable role for long non-coding RNAs and strengthened the contribution of autophagy as a major defense mechanism against mycobacteria. In this review, we summarize the history, epidemiological and clinical aspects of Buruli ulcer, focusing particularly on genetic findings relating to susceptibility to this disease. Finally, we discuss exciting new genetic avenues arising, in particular, from studies of mouse models, and the need for different disciplines to work together, to benefit from the extensive work on other mycobacterial diseases, mostly tuberculosis and leprosy. We are convinced that such pooling of effort will lead to the development of efficient novel strategies for combatting Buruli ulcer.
MeSH term(s)	Buruli Ulcer/epidemiology ; Buruli Ulcer/genetics ; Buruli Ulcer/microbiology ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Human Genetics ; Humans ; Mycobacterium ulcerans/physiology
Language	English
Publishing date	2020-04-07
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	223009-4
ISSN	1432-1203 ; 0340-6717
ISSN (online)	1432-1203
ISSN	0340-6717
DOI	10.1007/s00439-020-02163-1
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Article ; Online: A genome-wide perspective of human diversity and its implications in infectious disease.

Manry, Jérémy / Quintana-Murci, Lluis

Cold Spring Harbor perspectives in medicine

2013 Volume 3, Issue 1, Page(s) a012450

Abstract: Progress in genomic technologies, such as DNA arrays and next-generation sequencing, is allowing systematic characterization of the degree of human genetic variation at the scale of individual genomes. Public efforts, such as the International HapMap ... ...

Abstract	Progress in genomic technologies, such as DNA arrays and next-generation sequencing, is allowing systematic characterization of the degree of human genetic variation at the scale of individual genomes. Public efforts, such as the International HapMap Project and the 1000 Genomes Project, have provided a realistic picture of the levels of genetic diversity in individuals and populations. These genomic techniques are also making it possible to evaluate the contribution of host genetic diversity to differences in susceptibility to both rare and common infectious diseases. Recent studies have revealed the power of whole-exome sequencing for dissecting the immunological mechanisms underlying the pathogenesis of severe, rare infectious diseases. Likewise, genome-wide association studies on common viral, bacterial, and parasitic infections have shed light on the host genetic basis of susceptibility to infectious diseases and, in some cases, of disease progression and drug responses.
MeSH term(s)	Communicable Diseases/drug therapy ; Communicable Diseases/genetics ; Disease Progression ; Exome ; Gene Expression Profiling ; Genetic Predisposition to Disease ; Genetic Variation ; Genome, Human ; Genome-Wide Association Study/trends ; Humans ; Rare Diseases
Language	English
Publishing date	2013-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a012450
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Article: Génétique des populations et immunité chez l'homme - Le cas des interférons.

Manry, Jérémy / Quintana-Murci, Lluis

Medecine sciences : M/S

2012 Volume 28, Issue 12, Page(s) 1095–1101

Abstract: The evolutionary genetics dissection of immunity-related genes provides insights into immunological defence mechanisms and highlight host pathways playing an important role in pathogen resistance. Recent population genetic data have increased knowledge ... ...

Title translation	Population genetics and human immunity: the interferon paradigm.
Abstract	The evolutionary genetics dissection of immunity-related genes provides insights into immunological defence mechanisms and highlight host pathways playing an important role in pathogen resistance. Recent population genetic data have increased knowledge of the biological relevance of human interferons (IFN), cytokines released by host cells in response to pathogen presence or tumour cells. Some IFN-α subtypes as well as IFN-γ are strongly evolutionarily constrained, suggesting that the functions they fulfil are essential and non redundant. Other IFN, the most extreme cases being IFN-α10 and IFN-ε, can accumulate missense or nonsense mutations at high population frequencies, suggesting higher redundancy. Furthermore, genetic variation at some IFN genes can be advantageous for the host and increase in frequency by positive selection. This has been shown for type III IFN, where mutations at IL28A, IL28B and IL29 have been positively selected in Europeans and Asians, most likely by increasing resistance to viral infection. This review uses the IFN paradigm to illustrate the value of the evolutionary approach in highlighting important determinants of host immune responsiveness in the natural setting.
MeSH term(s)	Evolution, Molecular ; Genetic Heterogeneity ; Genetics, Population/methods ; Geography ; Host Specificity/genetics ; Host Specificity/immunology ; Humans ; Immunity/genetics ; Immunity/physiology ; Interferons/genetics ; Interferons/metabolism ; Interferons/physiology ; Models, Biological
Chemical Substances	Interferons (9008-11-1)
Language	French
Publishing date	2012-12
Publishing country	France
Document type	English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20122812020
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Article ; Online: Allele-dependent interaction of LRRK2 and NOD2 in leprosy.

Dallmann-Sauer, Monica / Xu, Yong Zhong / da Costa, Ana Lúcia França / Tao, Shao / Gomes, Tiago Araujo / Prata, Rhana Berto da Silva / Correa-Macedo, Wilian / Manry, Jérémy / Alcaïs, Alexandre / Abel, Laurent / Cobat, Aurélie / Fava, Vinicius M / Pinheiro, Roberta Olmo / Lara, Flavio Alves / Probst, Christian M / Mira, Marcelo T / Schurr, Erwin

PLoS pathogens

2023 Volume 19, Issue 3, Page(s) e1011260

Abstract: Leprosy, caused by Mycobacterium leprae, rarely affects children younger than 5 years. Here, we studied a multiplex leprosy family that included monozygotic twins aged 22 months suffering from paucibacillary leprosy. Whole genome sequencing identified ... ...

Abstract	Leprosy, caused by Mycobacterium leprae, rarely affects children younger than 5 years. Here, we studied a multiplex leprosy family that included monozygotic twins aged 22 months suffering from paucibacillary leprosy. Whole genome sequencing identified three amino acid mutations previously associated with Crohn's disease and Parkinson's disease as candidate variants for early onset leprosy: LRRK2 N551K, R1398H and NOD2 R702W. In genome-edited macrophages, we demonstrated that cells expressing the LRRK2 mutations displayed reduced apoptosis activity following mycobacterial challenge independently of NOD2. However, employing co-immunoprecipitation and confocal microscopy we showed that LRRK2 and NOD2 proteins interacted in RAW cells and monocyte-derived macrophages, and that this interaction was substantially reduced for the NOD2 R702W mutation. Moreover, we observed a joint effect of LRRK2 and NOD2 variants on Bacillus Calmette-Guérin (BCG)-induced respiratory burst, NF-κB activation and cytokine/chemokine secretion with a strong impact for the genotypes found in the twins consistent with a role of the identified mutations in the development of early onset leprosy.
MeSH term(s)	Child ; Humans ; Alleles ; Genetic Predisposition to Disease ; Genotype ; Leprosy/genetics ; Mutation ; Nod2 Signaling Adaptor Protein/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics
Chemical Substances	Nod2 Signaling Adaptor Protein ; NOD2 protein, human ; LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2023-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1011260
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Article ; Online: Allele-dependent interaction of LRRK2 and NOD2 in leprosy.

Monica Dallmann-Sauer / Yong Zhong Xu / Ana Lúcia França da Costa / Shao Tao / Tiago Araujo Gomes / Rhana Berto da Silva Prata / Wilian Correa-Macedo / Jérémy Manry / Alexandre Alcaïs / Laurent Abel / Aurélie Cobat / Vinicius M Fava / Roberta Olmo Pinheiro / Flavio Alves Lara / Christian M Probst / Marcelo T Mira / Erwin Schurr

PLoS Pathogens, Vol 19, Iss 3, p e

2023 Volume 1011260

Abstract	Leprosy, caused by Mycobacterium leprae, rarely affects children younger than 5 years. Here, we studied a multiplex leprosy family that included monozygotic twins aged 22 months suffering from paucibacillary leprosy. Whole genome sequencing identified three amino acid mutations previously associated with Crohn's disease and Parkinson's disease as candidate variants for early onset leprosy: LRRK2 N551K, R1398H and NOD2 R702W. In genome-edited macrophages, we demonstrated that cells expressing the LRRK2 mutations displayed reduced apoptosis activity following mycobacterial challenge independently of NOD2. However, employing co-immunoprecipitation and confocal microscopy we showed that LRRK2 and NOD2 proteins interacted in RAW cells and monocyte-derived macrophages, and that this interaction was substantially reduced for the NOD2 R702W mutation. Moreover, we observed a joint effect of LRRK2 and NOD2 variants on Bacillus Calmette-Guérin (BCG)-induced respiratory burst, NF-κB activation and cytokine/chemokine secretion with a strong impact for the genotypes found in the twins consistent with a role of the identified mutations in the development of early onset leprosy.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genome-wide association study of Buruli ulcer in rural Benin highlights role of two LncRNAs and the autophagy pathway.

Manry, Jeremy / Vincent, Quentin B / Johnson, Christian / Chrabieh, Maya / Lorenzo, Lazaro / Theodorou, Ioannis / Ardant, Marie-Françoise / Marion, Estelle / Chauty, Annick / Marsollier, Laurent / Abel, Laurent / Alcaïs, Alexandre

Communications biology

2020 Volume 3, Issue 1, Page(s) 177

Abstract: Buruli ulcer, caused by Mycobacterium ulcerans and characterized by devastating necrotizing skin lesions, is the third mycobacterial disease worldwide. The role of host genetics in susceptibility to Buruli ulcer has long been suggested. We conduct the ... ...

Abstract	Buruli ulcer, caused by Mycobacterium ulcerans and characterized by devastating necrotizing skin lesions, is the third mycobacterial disease worldwide. The role of host genetics in susceptibility to Buruli ulcer has long been suggested. We conduct the first genome-wide association study of Buruli ulcer on a sample of 1524 well characterized patients and controls from rural Benin. Two-stage analyses identify two variants located within LncRNA genes: rs9814705 in ENSG00000240095.1 (P = 2.85 × 10
MeSH term(s)	Adolescent ; Adult ; Autophagy/genetics ; Autophagy-Related Proteins/genetics ; Benin ; Buruli Ulcer/diagnosis ; Buruli Ulcer/genetics ; Buruli Ulcer/microbiology ; Case-Control Studies ; Child ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Host-Pathogen Interactions ; Humans ; Male ; Mutation, Missense ; Mycobacterium ulcerans/pathogenicity ; Phenotype ; Polymorphism, Single Nucleotide ; RNA, Long Noncoding/genetics ; Risk Assessment ; Risk Factors ; Young Adult
Chemical Substances	ATG16L1 protein, human ; Autophagy-Related Proteins ; RNA, Long Noncoding
Language	English
Publishing date	2020-04-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-020-0920-6
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Article ; Online: Genome-wide association study of Buruli ulcer in rural Benin highlights role of two LncRNAs and the autophagy pathway

Jeremy Manry / Quentin B. Vincent / Christian Johnson / Maya Chrabieh / Lazaro Lorenzo / Ioannis Theodorou / Marie-Françoise Ardant / Estelle Marion / Annick Chauty / Laurent Marsollier / Laurent Abel / Alexandre Alcaïs

Communications Biology, Vol 3, Iss 1, Pp 1-

2020 Volume 10

Abstract: Jeremy Manry, Quentin Vincent et al. report a genome-wide association study for susceptibility ...

Abstract	Jeremy Manry, Quentin Vincent et al. report a genome-wide association study for susceptibility to Buruli ulcer in a rural population from the West African country of Benin. They identify two independently associated variants within LncRNA genes and confirm the protective effect of a missense variant in the bacterial autophagy gene ATG16L1.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-04-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Skin-specific antibodies neutralizing mycolactone toxin during the spontaneous healing of

Foulon, Mélanie / Pouchin, Amélie / Manry, Jérémy / Khater, Fida / Robbe-Saule, Marie / Durand, Amandine / Esnault, Lucille / Delneste, Yves / Jeannin, Pascale / Saint-André, Jean-Paul / Croué, Anne / Altare, Frederic / Abel, Laurent / Alcaïs, Alexandre / Marion, Estelle

Science advances

2020 Volume 6, Issue 9, Page(s) eaax7781

Abstract: Buruli ulcer, a neglected tropical infectious disease, is caused ... ...

Abstract	Buruli ulcer, a neglected tropical infectious disease, is caused by
MeSH term(s)	Animals ; Antibodies, Neutralizing/immunology ; Bacterial Toxins/immunology ; Buruli Ulcer/immunology ; Buruli Ulcer/microbiology ; Immunoglobulin G/immunology ; Macrolides/immunology ; Mice ; Mycobacterium ulcerans/immunology ; Mycobacterium ulcerans/pathogenicity ; Skin/immunology ; Skin/microbiology
Chemical Substances	Antibodies, Neutralizing ; Bacterial Toxins ; Immunoglobulin G ; Macrolides ; mycolactone
Language	English
Publishing date	2020-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aax7781
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Article ; Online: Inborn errors of TLR3- or MDA5-dependent type I IFN immunity in children with enterovirus rhombencephalitis.

The Journal of experimental medicine

2021 Volume 218, Issue 12

Abstract: Enterovirus (EV) infection rarely results in life-threatening infection of the central nervous system. We report two unrelated children with EV30 and EV71 rhombencephalitis. One patient carries compound heterozygous TLR3 variants (loss-of-function ... ...

Abstract	Enterovirus (EV) infection rarely results in life-threatening infection of the central nervous system. We report two unrelated children with EV30 and EV71 rhombencephalitis. One patient carries compound heterozygous TLR3 variants (loss-of-function F322fs2* and hypomorphic D280N), and the other is homozygous for an IFIH1 variant (loss-of-function c.1641+1G>C). Their fibroblasts respond poorly to extracellular (TLR3) or intracellular (MDA5) poly(I:C) stimulation. The baseline (TLR3) and EV-responsive (MDA5) levels of IFN-β in the patients' fibroblasts are low. EV growth is enhanced at early and late time points of infection in TLR3- and MDA5-deficient fibroblasts, respectively. Treatment with exogenous IFN-α2b before infection renders both cell lines resistant to EV30 and EV71, whereas post-infection treatment with IFN-α2b rescues viral susceptibility fully only in MDA5-deficient fibroblasts. Finally, the poly(I:C) and viral phenotypes of fibroblasts are rescued by the expression of WT TLR3 or MDA5. Human TLR3 and MDA5 are critical for cell-intrinsic immunity to EV, via the control of baseline and virus-induced type I IFN production, respectively.
MeSH term(s)	Cells, Cultured ; Child, Preschool ; Encephalitis, Viral/genetics ; Encephalitis, Viral/immunology ; Enterovirus/drug effects ; Enterovirus/physiology ; Enterovirus Infections/genetics ; Enterovirus Infections/immunology ; Female ; Fibroblasts/drug effects ; Fibroblasts/immunology ; Fibroblasts/virology ; Humans ; Infant ; Interferon alpha-2/pharmacology ; Interferon-Induced Helicase, IFIH1/genetics ; Interferon-Induced Helicase, IFIH1/immunology ; Interferon-beta/immunology ; Interferon-beta/metabolism ; Loss of Function Mutation ; Male ; Metabolism, Inborn Errors/genetics ; Metabolism, Inborn Errors/immunology ; Poly I-C/pharmacology ; Rhombencephalon/virology ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/immunology ; Virus Replication/drug effects
Chemical Substances	Interferon alpha-2 ; Interferon-alpha2b ; TLR3 protein, human ; Toll-Like Receptor 3 ; Interferon-beta (77238-31-4) ; IFIH1 protein, human (EC 3.6.1.-) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2021-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20211349
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Article ; Online: Deciphering the genetic control of gene expression following Mycobacterium leprae antigen stimulation.

Manry, Jérémy / Nédélec, Yohann / Fava, Vinicius M / Cobat, Aurélie / Orlova, Marianna / Thuc, Nguyen Van / Thai, Vu Hong / Laval, Guillaume / Barreiro, Luis B / Schurr, Erwin

PLoS genetics

2017 Volume 13, Issue 8, Page(s) e1006952

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 ... ...

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.
MeSH term(s)	Antigens, Bacterial/immunology ; Down-Regulation ; Genetic Association Studies ; Genetic Predisposition to Disease ; Host-Pathogen Interactions/genetics ; Humans ; Leprosy/genetics ; Leprosy/immunology ; Mycobacterium leprae ; Polymorphism, Single Nucleotide ; Principal Component Analysis ; Quantitative Trait Loci ; RNA, Bacterial/isolation & purification ; Up-Regulation
Chemical Substances	Antigens, Bacterial ; RNA, Bacterial
Language	English
Publishing date	2017-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1006952
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