Publication: Association of IL1B -31C/T and IL1RA variable number of an 86-bp tandem repeat with dengue shock syndrome in Thailand
Issued Date
2014-07-01
Resource Type
ISSN
15376613
00221899
00221899
Other identifier(s)
2-s2.0-84904294294
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Infectious Diseases. Vol.210, No.1 (2014), 138-145
Suggested Citation
Areerat Sa-Ngasang, Jun Ohashi, Izumi Naka, Surapee Anantapreecha, Pathom Sawanpanyalert, Jintana Patarapotikul Association of IL1B -31C/T and IL1RA variable number of an 86-bp tandem repeat with dengue shock syndrome in Thailand. Journal of Infectious Diseases. Vol.210, No.1 (2014), 138-145. doi:10.1093/infdis/jiu042 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/34230
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Title
Association of IL1B -31C/T and IL1RA variable number of an 86-bp tandem repeat with dengue shock syndrome in Thailand
Abstract
Background. Dengue patients present a range of symptoms: dengue fever (DF), dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS). It is not clear whether this variability is due to their genetic background. Here we tested polymorphisms of interleukin 1 beta (IL1B) and interleukin 1 receptor antagonist (IL1RA) genes for association with DSS in the Thai population. Methods. Polymorphisms of IL1B -31C/T (rs1143627) and IL1RA 86-base-pair tandem repeat were analyzed in 871 patients (DF = 384, DHF = 413, and DSS = 74). Results. IL1B -31C and IL1RA 2/4 genotype were associated with DSS (IL1B -31C: DSS vs DHF: P = .0061, odds ratio [OR, 95% confidence interval {CI}], 3.49 [1.36-8.95]; DSS vs DF: P = .027, OR [95% CI], 2.81 [1.12-7.06]; IL1RA 2/4: DSS vs DHF: P = .017, OR [95% CI], 1.94 [1.12-3.40]; DSS vs DF: P = .024, OR [95% CI], 1.90 [1.07-3.4]). No difference was found between DF and DHF. Logistic regression analysis revealed that IL1B -31C and IL1RA 2/4 genotypes were each independently associated with DSS. Conclusions. Patients with IL1B -31C carrier, or IL1RA 2/4 genotype carry a risk for DSS, implying that IL1B may play a role in pathogenesis of DSS.