Littérature scientifique sur le sujet « Mycobacterium leprae – Vietnam »
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Articles de revues sur le sujet "Mycobacterium leprae – Vietnam"
Kai, M., N. H. Nguyen Phuc, H. A. Nguyen, T. H. B. D. Pham, K. H. Nguyen, Y. Miyamoto, Y. Maeda et al. « Analysis of Drug-Resistant Strains of Mycobacterium leprae in an Endemic Area of Vietnam ». Clinical Infectious Diseases 52, no 5 (2 février 2011) : e127-e132. http://dx.doi.org/10.1093/cid/ciq217.
Texte intégralKai, Masanori, Nhu Ha Nguyen Phuc, Thuy Huong Hoang Thi, An Hoang Nguyen, Yasuo Fukutomi, Yumi Maeda, Yuji Miyamoto et al. « Serological Diagnosis of Leprosy in Patients in Vietnam by Enzyme-Linked Immunosorbent Assay with Mycobacterium leprae-Derived Major Membrane Protein II ». Clinical and Vaccine Immunology 15, no 12 (22 octobre 2008) : 1755–59. http://dx.doi.org/10.1128/cvi.00148-08.
Texte intégralGilchrist, James J., Kathryn Auckland, Tom Parks, Alexander J. Mentzer, Lily Goldblatt, Vivek Naranbhai, Gavin Band et al. « Genome-wide association study of leprosy in Malawi and Mali ». PLOS Pathogens 18, no 9 (19 septembre 2022) : e1010312. http://dx.doi.org/10.1371/journal.ppat.1010312.
Texte intégralTam Chau, Ho Tinh, Phuc Nhu Ha Nguyen et Hoang Bach Nguyen. « Genotyping of Mycobacterium leprae strains in south central coast and central highlands of Vietnam ». Iranian Journal of Microbiology, 16 avril 2023. http://dx.doi.org/10.18502/ijm.v15i2.12470.
Texte intégralThèses sur le sujet "Mycobacterium leprae – Vietnam"
Gzara, Chaïma. « Génétique humaine de la lèpre au Vietnam : une histoire de familles ». Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5234.
Texte intégralLeprosy is a chronic infectious disease caused by Mycobacterium leprae. It primarily affects the skin and peripheral nerves, and can cause an irreversible impairment of nerve function, often leading to severe disabilities and social stigma if left untreated. The disease, re-qualified by WHO (World Health Organization) as a “Neglected Tropical Disease” in 2017, remains a major public health problem in regions of endemic countries, with over 200,000 new cases per year (one every two minutes). It is ranked second as the most common mycobacterial infectious disease, right after tuberculosis. While it has been well established that there is a genetic contribution to this disease, the underlying genetic causes remains unknown. In our study, we sought to reveal the host´s genetic architecture of leprosy by taking of a familial epidemiological approach. We conducted the first Family-Based Genome-Wide Association Study (GWAS) of leprosy in 481 Vietnamese nuclear families (parents and children) selected based on one affected child and collected over the past 20 years. Using this sample of 1,749 individuals, including 622 affected offspring, we performed association tests between six million biallelic genetic variants (Single-Nucleotide Polymorphism, genotyped or imputed) and the binary phenotype of disease status. Following this first analysis, we conducted a replication analysis of the most promising results in an independent sample of the same ethnic origin, accounting for 1,181 cases and 668 controls. The most significant results were observed within the HLA (Human Leukocyte Antigen) region, in which 3 independent SNPs displayed genome-wide significant associations. Among these, two were for the HLA class I region and one for the HLA class II (rs1265048 [OR = 0.69; p-value = 5.5x10⁻¹¹], rs114598080 [OR = 1.47; p-value = 8.8x10⁻¹³] and rs3187964 [OR = 1.67; p-value = 8.4x10⁻¹⁶] respectively). We also identified a missense variant in the LACC1 gene (rs3764147: OR = 1.52; p-value = 5.1x10⁻¹⁴) and an intergenic variant located close to the IL12B gene (rs6871626: OR = 0.73; p-value = 6.4x10⁻⁸). LACC1 encodes a central regulator of the metabolic function and bioenergetic state of macrophages and IL12B encodes IL-12p40, which is common to two interleukins, IL-12 and IL-23. Large GWAS are expensive, strongly limiting the number of variants to test in a replication set. Here, we took advantage of the available parental phenotypic and genotypic information to perform a classical case-control study among the parents of the family-based sample. Indeed, using of extensive computer simulations, we demonstrated that this population-based parental study is a valid, powerful and costless replication strategy to confirm family-based associations. Overall, our observations add to the attractiveness of family-based designs and should provide valuable help for investigators planning to perform GWA studies. Understanding leprosy pathophysiology infection is crucial to optimize preventive approaches based on genetic profiles. Dissection of the genetic control of the infection by M. leprae by its human host, therefore, constitutes an indispensable step. Finally, repositioning the family at the heart of the genetic quest means repositioning genetics into its natural environment