Cord blood gene expression in infants hospitalized with respiratory syncytial virus bronchiolitis

Hans-Olav Fjaerli1, Geir Bukholm, Camilla Skjaeret

  • 1Faculty Division, Department of Pediatrics, Akershus University Hospital, University of Oslo, Oslo, Norway. h.o.fjarli@medisin.uio.no

Insights

Respiratory Syncytial Virus (RSV) bronchiolitis in infants is linked to down-regulated genes FAM102A, TNFRSF25, and STMN3. A pathway regulating the actin cytoskeleton is also significantly reduced in affected infants.

Area of Science:

  • Immunology
  • Pediatrics
  • Genomics

Background:

  • Respiratory Syncytial Virus (RSV) exposure leads to varied infant outcomes, from asymptomatic infection to acute bronchiolitis.
  • Host, environmental, and viral factors likely influence disease severity in RSV infections.

Purpose of the Study:

  • To identify host genetic differences in infants hospitalized with RSV bronchiolitis compared to those with asymptomatic RSV infection.
  • To investigate specific gene expression patterns and pathways associated with severe RSV disease in neonates.

Main Methods:

  • Microarray analysis of cord blood from 5 infants with RSV bronchiolitis and 5 controls.
  • Quantitative Real-Time Polymerase Chain Reaction (QRT-PCR) validation of differentially expressed genes in 18 infants.
  • Gene Set Enrichment Analysis (GSEA) to identify dysregulated molecular pathways.

Main Results:

  • Microarray identified 15 significantly differentially expressed genes.
  • QRT-PCR confirmed down-regulation of FAM102A, TNFRSF25, and STMN3 in most infants with bronchiolitis.
  • GSEA revealed significant down-regulation of an actin cytoskeleton regulation pathway.

Conclusions:

  • The genes FAM102A, TNFRSF25, and STMN3 are down-regulated in infants hospitalized with RSV bronchiolitis.
  • A pathway involved in actin cytoskeleton regulation is also down-regulated in the cord blood of these infants.
  • These findings suggest a potential genetic component influencing RSV bronchiolitis severity.
Abstract

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