Abstract

BackgroundThe increased levels of blood cytokines is the main immunopathological process that were attributed to severe clinical outcomes in cases of influenza A, influenza B and people with influenza-like illness (ILI). Functional genetic polymorphisms caused by single nucleotide polymorphisms (SNPs) in inflammatory cytokines genes can influence their functions either qualitatively or quantitatively, which is associated with the possibility of severe influenza infections. The aim of the present case-control study was to investigate the association of polymorphisms in inflammatory cytokines genes with influenza patients and ILI group in an Iranian population.MethodsTotal number of 30 influenza B, 50 influenza A (H1N1) and 96 ILI inpatient individuals were confirmed by Real-time RT-PCR and HI assays. The genotype determination was assessed for defined SNPs in IL-1β, IL-17, IL-10 and IL-28 genes.ResultsThe frequencies of the IL-1β rs16944 (P = 0.007) and IL-17 rs2275913 (P = 0.006) genotypes were associated with severe influenza disease, while the frequencies of IL-10 rs1800872 and IL-28 rs8099917 were not associated with the disease (P > 0.05). Also, the absence of A allele in IL-17 rs2275913 SNP increased the risk of influenza A (H1N1) infection (P = 0.008).ConclusionsThis study demonstrated that influenza A- (H1N1) and B-infected patients and also ILI controls have different profiles of immune parameters, and individuals carrying the specific cytokine-derived polymorphisms may show different immune responses towards severe outcome.

Highlights

  • The increased levels of blood cytokines is the main immunopathological process that were attributed to severe clinical outcomes in cases of influenza A, influenza B and people with influenza-like illness (ILI)

  • Participants A total of 50 influenza A (H1N1), 30 influenza B and 96 ILI were participated in this study

  • In respect to age groups; 7 (14%) of influenza A (H1N1), 4 (13%) of influenza B groups and 16 (15%) of ILI cases were aged less than 20 years

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Summary

Introduction

The increased levels of blood cytokines is the main immunopathological process that were attributed to severe clinical outcomes in cases of influenza A, influenza B and people with influenza-like illness (ILI). Functional genetic polymorphisms caused by single nucleotide polymorphisms (SNPs) in inflammatory cytokines genes can influence their functions either qualitatively or quantitatively, which is associated with the possibility of severe influenza infections. Production and functional activity of inflammatory or anti-inflammatory cytokines sometimes originate from genetic variation such as single nucleotide polymorphisms (SNPs), altered coding region and promoter or regulatory region of cytokines genes. SNPs in certain alleles of proinflammatory cytokines resulted in susceptibility to a wide range of infections [9]. Regarding these cytokines, endothelial cells secrete Interleukin-1β (IL-1β) through NLRP3 inflammasome mechanisms that contribute to flu-induced inflammation in lung cells [10]. Another study highlighted the association of IgAN (IgA nephropathy; the most common form of primary glomerulonephritis) with upper respiratory tract infections [13]

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