ArticleThe Journal of infectious diseases2014
Associations between human leukocyte antigen class I variants and the Mycobacterium tuberculosis subtypes causing disease.
Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
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Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Pooled it
- Global variation in bacterial strains that cause tuberculosis disease: a systematic review and meta-analysis.BMC medicine · 2018Pooled it
- The association of class II HLA alleles with tuberculosis-associated immune reconstitution inflammatory syndrome.PLoS pathogens · 2025Trial
- Human Genetic Variation Associates With Infection by Derived Ugandan M. tuberculosis Lineage.The Journal of infectious diseases · 2026Article
- Insights into human history and complex traits from the genomes of African populations.Molecular biology and evolution · 2026Review
- Genetic Susceptibility to Tuberculosis and the Utility of Polygenic Scores in Population Stratification.International journal of molecular sciences · 2025Review
- Association of polymorphisms and abnormal methylation of several autophagy genes with pulmonary tuberculosis susceptibility, clinical manifestations in a Chinese population.BMC infectious diseases · 2025Observational
- The important roles of ERAP1, ERAP2 genes polymorphisms and their DNA methylation levels in pulmonary tuberculosis.BMC infectious diseases · 2025Article
- Article
- The immunogenetics of tuberculosis (TB) susceptibility.Immunogenetics · 2023Review
- Human and pathogen genotype-by-genotype interactions in the light of coevolution theory.PLoS genetics · 2023Review
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- Article
- Interaction betweenPathogens (Basel, Switzerland) · 2021Article
- Local adaptation in populations ofF1000Research · 2021Article
- Genetic Analysis of TB Susceptibility Variants in Ghana Reveals Candidate Protective Loci inFrontiers in genetics · 2021Article
- A natural polymorphism of Mycobacterium tuberculosis in the esxH gene disrupts immunodomination by the TB10.4-specific CD8 T cell response.PLoS pathogens · 2020Article
- Genetics and evolution of tuberculosis pathogenesis: New perspectives and approaches.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020Review
- Interaction between host genes and Mycobacterium tuberculosis lineage can affect tuberculosis severity: Evidence for coevolution?PLoS genetics · 2020Article
- The Interplay of Human andFrontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe development of active tuberculosis disease has been shown to be multifactorial. Interactions between host and bacterial genotype may influence disease outcome, with some studies indicating the adaptation of M. tuberculosis strains to specific human populations. Here we investigate the role of the human leukocyte antigen (HLA) class I genes in this biological process.
methodsThree hundred patients with tuberculosis from South Africa were typed for their HLA class I alleles by direct sequencing. Mycobacterium tuberculosis genotype classification was done by IS6110 restriction fragment length polymorphism genotyping and spoligotyping.
resultsWe showed that Beijing strain occurred more frequently in individuals with multiple disease episodes (P < .001) with the HLA-B27 allele lowering the odds of having an additional episode (odds ratio, 0.21; P = .006). Associations were also identified for specific HLA types and disease caused by the Beijing, LAM, LCC, and Quebec strains. HLA types were also associated with disease caused by strains from the Euro-American or East Asian lineages, and the frequencies of these alleles in their sympatric human populations identified potential coevolutionary events between host and pathogen.
conclusionsThis is the first report of the association of human HLA types and M. tuberculosis strain genotype, highlighting that both host and pathogen genetics need to be taken into consideration when studying tuberculosis disease development.
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