Correlation of METTL4 genetic variants and severe pneumonia pediatric patients in Southern China

Liuheyi Ma1, Xiaoyu Zuo2, Bingtai Lu3,4

  • 1School of Medicine, South China University of Technology, Guangzhou, 510006, China.

BMC Genomic Data
|May 1, 2025
PubMed

Insights

Genetic variations in the METTL4 gene are linked to increased severe pneumonia risk in children. This study identifies METTL4 as a potential predisposing gene for pediatric severe pneumonia.

Area of Science:

  • Genetics
  • Pediatrics
  • Molecular Biology

Background:

  • Pneumonia poses a significant global health burden in children under five.
  • The genetic factors contributing to pneumonia susceptibility are not well understood.
  • Methyltransferase 4, N6-adenosine (METTL4) is involved in RNA/DNA methylation and activated under hypoxia.

Purpose of the Study:

  • To investigate the association between genetic variations in the METTL4 gene and severe pneumonia risk in children.
  • To identify specific single nucleotide polymorphisms (SNPs) within METTL4 that may predispose individuals to severe pneumonia.

Main Methods:

  • A cohort study involving 1034 children with severe pneumonia and 8426 healthy controls.
  • Analysis of candidate regulatory single nucleotide polymorphisms (SNPs) within the METTL4 gene.
  • Utilized expression quantitative trait loci (eQTLs), RegulomeDB, and FORGEdb to assess SNP regulatory potential in lung tissue.

Main Results:

  • The C allele of rs9989554 was significantly associated with an increased risk of severe pneumonia (P=0.00023, OR=1.21).
  • The G allele of rs16943442 also showed a significant association with increased severe pneumonia risk (P=0.0026, OR=1.22).
  • Both identified SNPs demonstrated regulatory potential in lung tissue.

Conclusions:

  • This study is the first to link genetic variations in METTL4 to severe pneumonia susceptibility in pediatric populations.
  • METTL4 is identified as a novel predisposing gene for severe pneumonia.
  • Further research is needed to validate these findings and explore the biological mechanisms of METTL4 in severe pneumonia.
Abstract

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