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Association between interferon lambda 3 rs12979860 polymorphism and clinical outcome in dengue virus‐infected children
Author(s) -
Silva Cezar Renata Duarte,
Silva Castanha Priscila Mayrelle,
Matos Freire Naishe,
Mola Carla,
Feliciano do Carmo Rodrigo,
Tenório Cordeiro Marli,
Baptista Paulo,
Silva Vasconcelos Luydson Richardson,
Moura Patrícia,
Silva Teixeira Vanessa Gabryelle
Publication year - 2020
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12477
Subject(s) - dengue fever , genotype , dengue virus , allele , single nucleotide polymorphism , snp , immunology , medicine , virology , biology , gene , genetics
Single nucleotide polymorphisms (SNPs) in immune‐related genes have been shown to play a role in driving the development of the severe phenotypes of dengue virus (DENV) infection. We assessed the association between IFNL3 gene SNP (rs12979860) and dengue clinical outcomes in children. Patients with dengue‐related symptoms (aged 1–15 years) admitted at a public hospital in Northeast Brazil were invited to participate. The association between rs12979860 polymorphism and dengue classification and clinical signs and symptoms were analysed. A total of 206 DENV‐infected children were included: 53.4% of the infections were classified as severe dengue. The T allele carriers had higher risk of developing severe dengue when compared to CC genotype carriers (OR: 1.81; 95% CI: 0.98–3.32 p = .054). The T allele carriers also showed longer fever episodes when compared to patients with the CC genotype (OR: 1.90; 95%CI: 1.07–3.38; p = .027). On the other hand, the ones carrying the CT/TT genotype had 70% lower chance of developing thrombocytopenia when compared to those with the CC genotype (OR: 0.30; 95%CI: 0.08–0.88; p = .042). Our findings demonstrated that the T allele carriers of the IFNL3 gene had higher risk of developing severe dengue, suggesting a link between IFN‐λ expression and DENV immunopathogenesis.