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Updated: Aug 17, 2026
High-Throughput Transcriptome Analysis for Investigating Host-Pathogen Interactions
Published on: March 5, 2022
Bulk transcriptomics of peripheral blood mononuclear cells delineates systems-level immune dysregulation in pediatric
Abdul R Anshad1, Muthuvel Atchaya1, Amudhan Murugesan2
1Infection and Inflammation, Department of Biotechnology, Central University of Tamil Nadu, Thiruvarur, India.
Insights
Pediatric dengue reveals significant gene expression changes, particularly in immune pathways. Secondary infections show signs of immune exhaustion, highlighting key molecular differences in children with dengue.
Area of Science:
- Immunology
- Genomics
- Pediatrics
Background:
- Children face higher risks of severe dengue, but the underlying molecular reasons are unclear.
- Understanding pediatric dengue pathogenesis is crucial for improving outcomes.
Purpose of the Study:
- To investigate the transcriptomic landscape of pediatric dengue.
- To identify immune determinants contributing to severe disease in children.
Main Methods:
- RNA sequencing (RNA-Seq) was performed on peripheral blood mononuclear cells (PBMCs).
- Analysis included differential gene expression (DEG) and pathway analysis.
- Compared primary dengue, secondary dengue, and healthy pediatric controls.
Main Results:
- Pediatric dengue showed extensive transcriptional alterations, including complement cascade, macrophage-associated genes, and immune checkpoint molecules.
- Secondary dengue infections exhibited significant changes in immune checkpoints and macrophage activation genes, suggesting immune exhaustion.
- Immune checkpoint genes consistently differed between primary and secondary dengue cohorts.
Conclusions:
- Transcriptomic signatures in pediatric dengue offer preliminary insights into disease pathogenesis.
- Dysregulated gene expression patterns require further functional validation.
- Findings highlight potential molecular mechanisms behind heightened susceptibility and disease severity in children.
Abstract:
Children are disproportionately at a greater risk of developing severe dengue disease, yet the molecular mechanisms driving the heightened susceptibility remains poorly understood. To elucidate the immune determinants of pediatric dengue pathogenesis, we profiled the transcriptomic landscape by performing RNA sequencing (RNA-Seq) on peripheral blood mononuclear cells (PBMCs) from laboratory-confirmed cases of primary and secondary pediatric dengue, as well as pediatric healthy controls. Differential gene expression (DEG) and pathway analyses were performed to delineate the transcriptional alterations. Pediatric dengue was marked by extensive transcriptional changes with altered expression of genes associated with the complement cascade macrophage-associated genes as well as immune checkpoint molecules. Notably, secondary infection had significant alterations in immune checkpoint molecules and genes associated with macrophage activation, suggesting the onset of immune exhaustion during reinfection. Differences between the primary and secondary dengue cohorts were modest relative to the transcriptional differences observed between either of the groups and healthy controls, with immune checkpoint genes showing the most consistent divergence between the two dengue cohorts. While our initial findings provide early insights into the transcriptional patterns potentially associated with disease outcomes, the dysregulated transcriptomic signatures reported here are preliminary requiring systemic functional validation to determine their biologic role in the immunopathogenesis of pediatric dengue infection.
