ArticleNature genetics2010
Genome-wide association study identifies variants in the CFH region associated with host susceptibility to meningococcal disease.
Article in Nature genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 6 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
137 citing papers in PubMed, 6 syntheses or guidelines pooled it, 287 citations in OpenAlex.
- Interleukin gene polymorphisms and susceptibility to HIV-1 infection: a meta-analysis.Journal of genetics · 2018Pooled it
- Natural resistance to Meningococcal Disease related to CFH loci: Meta-analysis of genome-wide association studies.Scientific reports · 2016Pooled it
- Association of complement receptor 2 polymorphisms with innate resistance to HIV-1 infection.Genes and immunity · 2015Pooled it
- Genome-wide and gene-centric analyses of circulating myeloperoxidase levels in the charge and care consortia.Human molecular genetics · 2013Pooled it
- Genome-wide association analyses identify three new susceptibility loci for primary angle closure glaucoma.Nature genetics · 2012Pooled it
- The interleukin-6 receptor as a target for prevention of coronary heart disease: a mendelian randomisation analysis.Lancet (London, England) · 2012Pooled it
- Adults with septic shock and extreme hyperferritinemia exhibit pathogenic immune variation.Genes and immunity · 2019Trial
- Association of coding and UTR variants in the known regions with wet age-related macular degeneration in Han Chinese population.Journal of human genetics · 2018Trial
- Genome-wide association study of paediatric bacteraemia and sepsis.EBioMedicine · 2026Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- Epidemiology and genetic diversity of invasive Neisseria meningitidis strains circulating in Portugal from 2003 to 2020.International microbiology : the official journal of the Spanish Society for Microbiology · 2024Article
- A common NFKB1 variant detected through antibody analysis in UK Biobank predicts risk of infection and allergy.American journal of human genetics · 2024Article
- Role of factor H-related protein 3 inFrontiers in immunology · 2024Article
- Genetic variants linked to the phenotypic outcome of invasive disease and carriage ofMicrobial genomics · 2023Article
- Meningococcal factor H-binding protein: implications for disease susceptibility, virulence, and vaccines.Trends in microbiology · 2023Review
- Genetic variability shapes the alternative pathway complement activity and predisposition to complement-related diseases.Immunological reviews · 2023Review
- The first case report of complement component 7 deficiency in Qatar and a 10-year follow-up.Frontiers in immunology · 2023Article
- PathogenicInfection and immunity · 2022Article
- Variation in CFHR3 determines susceptibility to meningococcal disease by controlling factor H concentrations.American journal of human genetics · 2022Article
- Article
77 more citing papers are in PubMed but not listed here.
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22 authors at 10 institutions in 6 countries.
Funding
Abstract
Meningococcal disease is an infection caused by Neisseria meningitidis. Genetic factors contribute to host susceptibility and progression to disease, but the genes responsible for disease development are largely unknown. We report here a genome-wide association study for host susceptibility to meningococcal disease using 475 individuals with meningococcal disease (cases) and 4,703 population controls from the UK. We performed, in Western European and South European cohorts (consisting of 968 cases and 1,376 controls), two replication studies for the most significant SNPs. A cluster of complement factor SNPs replicated independently in both cohorts, including SNPs within complement factor H (CFH) (rs1065489 (p.936D<E), P = 2.2 x 10(-11)) and in CFH-related protein 3 (CFHR3)(rs426736, P = 4.6 x 10(-13)). N. meningitidis is known to evade complement-mediated killing by the binding of host CFH to the meningococcal factor H-binding protein (fHbp). Our study suggests that host genetic variation in these regulators of complement activation plays a role in determining the occurrence of invasive disease versus asymptomatic colonization by this pathogen.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.