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* Molecular Parasitology Laboratory, Australian Centre for International and Tropical Health and Nutrition, Queensland Institute of Medical Research and University of Queensland, Australia;
Molecular Epidemiology Laboratories, Queensland Institute of Medical Research, Brisbane, Australia;
Jiangxi Provincial Institute of Parasitic Diseases, Nanchang, People’s Republic of China; and
Hunan Institute of Parasitic Diseases, World Health Organization Collaborating Centre for Research and Control on Schistosomiasis in Lake Region, Yueyang, Hunan Province, People’s Republic of China
Genetic studies of human susceptibility to Schistosoma (blood fluke) infections have previously identified a genetic locus determining infection intensity with the African species, Schistosoma mansoni, in the 5q31–33 region of the human genome that is known to contain the Th2 immune response cluster, including the genes encoding the IL-4, IL-5, and IL-13 cytokines. These cytokines are key players in inflammatory immune responses and have previously been implicated in human susceptibility to infection with the Asian species, S. japonicum. In a nested case control study, we genotyped 30 HapMap tagging single nucleotide polymorphisms (SNPs) across these three genes in 159 individuals identified as putatively susceptible to reinfection with S. japonicum and in 133 putatively resistant individuals. A third group comprising 113 individuals demonstrating symptomatic infection was also included. The results provided no significant association at a global level between reinfection predisposition and any of the individual SNPs or haplotype blocks. However, two tagging SNPs in IL-5 demonstrated globally significant association with susceptibility to symptomatic infection. They were in strong linkage disequilibrium with each other and were found to belong to the same haplotype block that also provided a significant association after permutation testing. This haplotype was located in the 3'-untranslated region of IL-5, suggesting that variants in this region of IL-5 may modulate the immune response in these individuals with symptomatic infection.
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1 This study was supported by the National Institute of Allergy and Infectious Diseases (NIAID) (Tropical Medicine Research Center Grant 1 P 50AI-39461) and a National Health and Medical Research Council of Australia and Wellcome Trust (U.K.) International Collaborative Research Grants Scheme Award.
2 Address correspondence and reprint requests to Dr. Magda Ellis, Molecular Parasitology Laboratory, Australian Centre for International and Tropical Health and Nutrition, The Queensland Institute of Medical Research, 300 Herston Road, Herston, Brisbane, Queensland 4029, Australia. E-mail address: Magda.Ellis{at}qimr.edu.au
3 Abbreviations used in this paper: SNP, single nucleotide polymorphism; CI, confidence interval; LD, linkage disequilibrium; LOD, logarithm of odds; UTR, untranslated region.
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