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Comparative clinical transcriptome of pir genes in severe Plasmodium vivax malaria

Pon Arunachalam Boopathi1, Saurabh Singh1, Priyanka Roy1

  • 1Molecular Parasitology and Systems Biology Laboratory, Department of Biological Sciences, Birla Institute of Technology and Science, Pilani Campus, Pilani, Rajasthan, India.

Plos Neglected Tropical Diseases
|February 18, 2026
PubMed

Insights

Severe Plasmodium vivax malaria involves specific pir genes. Transcriptomic analysis revealed distinct pir gene upregulation in cerebral malaria and hepatic dysfunction, highlighting their role in severe disease.

Area of Science:

  • Molecular Biology
  • Genetics
  • Parasitology

Background:

  • Plasmodium vivax, often considered benign, causes severe manifestations like hepatic dysfunction and cerebral malaria.
  • The Plasmodium interspersed repeat (pir) gene superfamily, including vir genes, is implicated in parasite cyto-adherence and immune evasion.
  • Understanding pir gene expression is crucial for addressing the public health challenge posed by P. vivax malaria.

Purpose of the Study:

  • To compare the transcriptomes of P. vivax parasites from severe malaria cases (hepatic dysfunction, cerebral malaria) with uncomplicated cases.
  • To identify differentially expressed pir genes, particularly focusing on their role in severe P. vivax manifestations.
  • To investigate the specific pir subfamilies upregulated in cerebral malaria and hepatic dysfunction.

Main Methods:

  • Transcriptomic analysis using custom-designed microarrays.
  • Isolation and hybridization of RNA from P. vivax parasites from 23 Indian patients (6 uncomplicated, 12 hepatic dysfunction, 5 cerebral malaria).
  • Differential gene expression analysis focusing on pir gene subfamilies.

Main Results:

  • A wide range of pir subfamilies were differentially expressed in severe malaria patients.
  • Upregulation of 24 pir genes in the cerebral malaria group and 28 pir genes in the hepatic dysfunction group was observed.
  • Specific pir subfamilies, including vir subfamily E, pvpir subfamily H (cerebral malaria), and vir subfamilies E and C (hepatic dysfunction), showed distinct proportional expression patterns.

Conclusions:

  • The study identifies specific pir genes and subfamilies that are upregulated in severe Plasmodium vivax malaria.
  • Differential expression patterns of pir genes in cerebral malaria and hepatic dysfunction suggest their involvement in disease pathogenesis.
  • These findings contribute to understanding the molecular mechanisms underlying severe P. vivax malaria and may inform future therapeutic strategies.

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