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Host cell entry by apicomplexa parasites requires actin polymerization in the host cell

Virginie Gonzalez1, Audrey Combe, Violaine David

  • 1Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), Paris, France.

Cell Host & Microbe
|March 17, 2009
PubMed

Insights

Host cell invasion by Apicomplexa parasites, like Toxoplasma gondii and Plasmodium, actively involves host actin. This study reveals a crucial role for host actin polymerization in parasite entry.

Area of Science:

  • Parasitology
  • Cell Biology
  • Molecular Biology

Background:

  • Apicomplexa are obligate intracellular parasites.
  • Parasite invasion relies on a motor complex and a moving junction.
  • Host actin's role in invasion was previously considered minimal.

Purpose of the Study:

  • To investigate the role of host actin in Apicomplexa invasion.
  • To elucidate the molecular mechanisms of host cell entry by Apicomplexa.

Main Methods:

  • Utilized Toxoplasma gondii tachyzoites and Plasmodium berghei sporozoites.
  • Observed host cell invasion dynamics using microscopy.
  • Analyzed the involvement of actin and the Arp2/3 complex.

Main Results:

  • Demonstrated host actin's active participation in parasite entry.
  • Identified a stable, ring-shaped F-actin structure at the parasite-host junction.
  • Showed recruitment of the Arp2/3 complex to the actin ring, essential for invasion.

Conclusions:

  • Apicomplexa invasion requires both the parasite's motor and host actin polymerization.
  • Host actin anchors the moving junction, facilitating parasite penetration.
  • This finding challenges previous models of Apicomplexa invasion.

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