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Nuclear import of malaria RNA rewires splicing in host immune cells

Paula Abou Karam1, Edo Kiper1, Tamar Ziv2

  • 1Department of Biomolecular Sciences, Faculty of Biochemistry, Weizmann Institute of Science, Rehovot, Israel.

Cell Reports
|February 14, 2026
PubMed

Insights

The malaria parasite Plasmodium falciparum uses its own RNA molecules to disrupt host immune cell function. These parasite RNAs invade host cell nuclei, interfering with essential RNA processing and altering immune responses.

Area of Science:

  • Molecular biology
  • Immunology
  • Parasitology

Background:

  • Eukaryotic pathogens manipulate host immunity through various strategies.
  • RNA-based virulence mechanisms are not well understood.
  • The malaria parasite Plasmodium falciparum is a significant global health concern.

Purpose of the Study:

  • To elucidate the RNA-based virulence mechanisms employed by Plasmodium falciparum.
  • To investigate how parasite-derived transcripts interfere with host immune responses.

Main Methods:

  • Analysis of Plasmodium falciparum mRNAs exported from infected red blood cells.
  • Investigation of nuclear import of parasite transcripts into host immune cells.
  • Identification of host RNA-binding proteins interacting with parasite transcripts using biochemical assays.
  • Assessment of host splicing regulation and gene expression changes.

Main Results:

  • Plasmodium falciparum mRNAs are imported into host cell nuclei.
  • Parasite transcripts bind host splicing factors ACIN1 and PNN.
  • This interaction disrupts host RNA splicing, leading to widespread transcript misprocessing.
  • Altered expression of immune-related proteins in host cells was observed.

Conclusions:

  • Plasmodium falciparum utilizes a novel RNA-based strategy to manipulate host immunity.
  • Parasite transcripts hijack host nuclear RNA processing machinery.
  • This mechanism reshapes host transcript isoform landscapes and immune signaling pathways.
Keywords:
ACIN1CP: microbiologyCP: molecular biologyPNNcell-cell communicationextracellular RNAextracellular vesicleshost-pathogen interactionmalariasplicingsplicing dysregulation

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