ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2015
Single nucleotide polymorphisms in immune response genes in acute Q fever cases with differences in self-reported symptoms.
Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 10 citations in OpenAlex.
- Host Genetic Factors in Q Fever Susceptibility.Pathogens (Basel, Switzerland) · 2025Article
- Seroprevalence and risk factors for Q fever and Rift Valley fever in pastoralists and their livestock in Afar, Ethiopia: A One Health approach.PLoS neglected tropical diseases · 2024Article
- Natural genetic variation in Drosophila melanogaster reveals genes associated with Coxiella burnetii infection.Genetics · 2021Article
- Cytokine Gene Polymorphisms Associated With Symptom Clusters in Oncology Patients Undergoing Radiation Therapy.Journal of pain and symptom management · 2017Article
- Observational
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9 authors at 4 institutions in 1 country.
Funding
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Abstract
Genes involved in human immune response are well recognized to influence the clinical course of infection. The association of host genetics with susceptibility to and severity of clinical symptoms in acute Q fever was investigated. Single nucleotide polymorphisms (SNPs) in the IFNG (rs2430561/rs1861493), STAT1 (rs1914408), and VDR (rs2228570) genes were determined in 85 patients from the 2007 Dutch acute Q fever outbreak, and a symptom score was calculated. IFNG rs1861493 showed a significant association with the symptom score; IFNG rs2430561 showed a similar trend. These SNPs were then used to reproduce results in a 2009 outbreak population (n = 123). The median symptom score differed significantly in both populations: 2 versus 7. The significant association of IFNG rs1861493 with symptom score in the first population was not reproduced in the second population. We hypothesize that individuals in the second outbreak were exposed to a higher Coxiella burnetii dose compared to the first, which overruled the protection conferred by the A-allele of IFNG rs1861493 in the first population.
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