Association of interleukin 18, interleukin 2, and tumor necrosis factor polymorphisms with subacute sclerosing

Ibrahim Etem Piskin1, Sevim Karakas-Celik, Mustafa Calik

  • 1Department of Pediatrics, Bulent Ecevit University Faculty of Medicine, Zonguldak, Turkey.

Insights

Genetic variations in the interleukin-18 (IL-18) gene may increase the risk of developing subacute sclerosing panencephalitis (SSPE), a rare measles virus-induced brain disorder.

Area of Science:

  • Immunogenetics
  • Neuroscience
  • Virology

Background:

  • Subacute sclerosing panencephalitis (SSPE) is a progressive, fatal neurological disorder caused by measles virus (MV) infection.
  • The exact mechanisms linking MV infection to SSPE pathogenesis remain unclear, with host genetic factors playing a potential role.
  • Previous research suggests that specific gene polymorphisms may impair the host's ability to clear MV, contributing to SSPE development.

Purpose of the Study:

  • To investigate the association between polymorphisms in interleukin (IL)-2, IL-18, and tumor necrosis factor alpha (TNF-α) genes and the risk of developing SSPE.
  • To identify potential genetic risk factors influencing the host's susceptibility to MV-induced SSPE.

Main Methods:

  • Single-nucleotide polymorphisms (SNPs) in the promoter regions of IL-2 (-330), TNF-α (-308), and IL-18 (-137 and -607) were analyzed.
  • Genotyping was performed using polymerase chain reaction with sequence-specific primers.
  • The study included 54 SSPE patients and 72 healthy controls.

Main Results:

  • A significantly higher frequency of the AA genotype at IL-18 position -607 was observed in SSPE patients compared to controls (p<0.001, OR: 5.76).
  • SSPE patients showed a significantly higher proportion of the C allele at IL-18 position -137 (p=0.002, OR: 2.72).
  • Haplotype analysis revealed a significantly higher frequency of the CA haplotype in the IL-18 gene among SSPE patients (p<0.001, OR: 3.99). No significant associations were found for IL-2 and TNF-α polymorphisms.

Conclusions:

  • Polymorphisms in the IL-18 gene, specifically at positions -607 and -137, are suggested as potential genetic risk factors for SSPE.
  • These findings contribute to understanding the genetic underpinnings of SSPE susceptibility.
  • Further research is warranted to elucidate the precise role of IL-18 in SSPE pathogenesis.