Association of polymorphisms in inflammatory cytokines encoding genes with severe cases of influenza A/H1N1 and B in an Iranian population

Abstract

Background 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. 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. Methods Total 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. Results The 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 ). Conclusions This 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.

Metabolic host response and therapeutic approaches to influenza infection

“…In another study, an association between IL-1β rs16944 and IL-17 rs2275913 genotypes and severe influenza disease was found while IL-10 rs1800872 and IL-28 rs8099917 polymorphisms were not associated with influenza disease. Also, lacking an A allele in IL-17 rs2275913 could increase the risk of influenza A (H1N1) infection [2]. Such polymorphisms in immune system genes may be associated with some metabolic changes and, in turn, may reinforce the metabolic disorders following influenza infection.…”

“…Influenza virus infection (IVI) is one of the most common infectious agents, capable of infecting a variety of avian and mammalian species. The virus is responsible for seasonal epidemics, leading to 3-5 million severe infections and 250,000-500,000 deaths annually [1,2]. Despite the annual vaccination program, the high mortality rate caused by influenza infection and its various complications, including chronic lung disease, cardiac disease, asthma, and metabolic disorders, is yet to be adequately addressed [3][4][5].…”

Role of the Host Genetic Susceptibility to 2009 Pandemic Influenza A H1N1

“…In contrast, the rs3136558 CC genotype was associated with an increased risk, but rs16944 AG and rs3136558 TC were associated with a decreased risk of infection [ 104 ]. In an Iranian population, the rs16944 was associated with severe influenza disease [ 109 ]. In a Chinese population, the rs1143627 ( IL1B ) and rs17561 ( IL1A ) were found to be associated with susceptibility to A H1N1 pdm09 [ 110 ].…”

Galectin-1 Ameliorates Influenza A H1N1pdm09 Virus-Induced Acute Lung Injury

“…We also found that IL-1β, IL-6, IL-10, MCP-1, MIP-1α and RANTES in mouse BALF decreased along with reduced BALF cells after Gal-1 treatment. These cytokines are reported to increase in IAV infection and are associated with increased disease severity and affect the outcome of influenza patients (Garcia-Ramirez et al, 2015;Guo et al, 2015;Keshavarz et al, 2019). Among them, MCP-1, IL-1β, IL-6 and MIP-1α are mainly secreted by macrophages during IAV infection .…”