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Malaria parasites both repress host CXCL10 and use it as a cue for growth acceleration

Author

Listed:
  • Yifat Ofir-Birin

    (Weizmann Institute of Science)

  • Hila Ben Ami Pilo

    (Weizmann Institute of Science)

  • Abel Cruz Camacho

    (Weizmann Institute of Science)

  • Ariel Rudik

    (Weizmann Institute of Science)

  • Anna Rivkin

    (Weizmann Institute of Science)

  • Or-Yam Revach

    (Weizmann Institute of Science)

  • Netta Nir

    (Weizmann Institute of Science)

  • Tal Block Tamin

    (Weizmann Institute of Science)

  • Paula Abou Karam

    (Weizmann Institute of Science)

  • Edo Kiper

    (Weizmann Institute of Science)

  • Yoav Peleg

    (Weizmann Institute of Science)

  • Reinat Nevo

    (Weizmann Institute of Science)

  • Aryeh Solomon

    (Weizmann Institute of Science)

  • Tal Havkin-Solomon

    (Weizmann Institute of Science)

  • Alicia Rojas

    (Weizmann Institute of Science)

  • Ron Rotkopf

    (Weizmann Institute of Science)

  • Ziv Porat

    (Weizmann Institute of Science)

  • Dror Avni

    (Sheba Medical Center
    Tel Aviv University)

  • Eli Schwartz

    (Sheba Medical Center
    Tel Aviv University)

  • Thomas Zillinger

    (University Hospital Bonn)

  • Gunther Hartmann

    (University Hospital Bonn)

  • Antonella Pizio

    (Technical University of Munich)

  • Neils Ben Quashie

    (University of Ghana
    University of Ghana Medical School)

  • Rivka Dikstein

    (Weizmann Institute of Science)

  • Motti Gerlic

    (Tel Aviv University)

  • Ana Claudia Torrecilhas

    (Federal University of São Paulo, UNIFESP)

  • Carmit Levy

    (Tel Aviv University)

  • Esther N. M. Nolte-‘t Hoen

    (Faculty of Veterinary Medicine, Utrecht University)

  • Andrew G. Bowie

    (Trinity Biomedical Sciences Institute, Trinity College Dublin)

  • Neta Regev-Rudzki

    (Weizmann Institute of Science)

Abstract

Pathogens are thought to use host molecular cues to control when to initiate life-cycle transitions, but these signals are mostly unknown, particularly for the parasitic disease malaria caused by Plasmodium falciparum. The chemokine CXCL10 is present at high levels in fatal cases of cerebral malaria patients, but is reduced in patients who survive and do not have complications. Here we show a Pf ‘decision-sensing-system’ controlled by CXCL10 concentration. High CXCL10 expression prompts P. falciparum to initiate a survival strategy via growth acceleration. Remarkably, P. falciparum inhibits CXCL10 synthesis in monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The underlying inhibition cascade involves RNA cargo delivery into monocytes that triggers RIG-I, which leads to HUR1 binding to an AU-rich domain of the CXCL10 3’UTR. These data indicate that when the parasite can no longer keep CXCL10 at low levels, it can exploit the chemokine as a cue to shift tactics and escape.

Suggested Citation

  • Yifat Ofir-Birin & Hila Ben Ami Pilo & Abel Cruz Camacho & Ariel Rudik & Anna Rivkin & Or-Yam Revach & Netta Nir & Tal Block Tamin & Paula Abou Karam & Edo Kiper & Yoav Peleg & Reinat Nevo & Aryeh Sol, 2021. "Malaria parasites both repress host CXCL10 and use it as a cue for growth acceleration," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24997-7
    DOI: 10.1038/s41467-021-24997-7
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