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ZAP-70 kinase regulates HIV cell-to-cell spread and virological synapse formation

Nathalie Sol-Foulon1, Marion Sourisseau, Françoise Porrot

  • 1Groupe Virus et Immunité, Institut Pasteur, CNRS URA1930, France.

The EMBO Journal
|January 12, 2007
PubMed

Insights

The study reveals that ZAP-70 kinase is crucial for efficient human immunodeficiency virus (HIV) replication and spread. Without ZAP-70, HIV transmission between cells and the formation of virological synapses are significantly impaired.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Human immunodeficiency virus (HIV) spreads efficiently in lymphocytes, often via virological synapses (VSs).
  • The cellular proteins forming these VSs are not fully understood, despite similarities to immunological synapses.

Purpose of the Study:

  • To investigate the role of ZAP-70, a T-cell activation kinase, in HIV replication and cell-to-cell transmission.
  • To elucidate how ZAP-70 influences the formation of virological synapses during HIV infection.

Main Methods:

  • Examined HIV replication in lymphocytes with and without functional ZAP-70.
  • Analyzed viral cycle steps, intracellular Gag localization, and cell-to-cell transmission.
  • Assessed the formation of virological synapses in the presence or absence of ZAP-70.

Main Results:

  • HIV replication was significantly delayed in ZAP-70 deficient lymphocytes.
  • ZAP-70 was not essential for early viral entry or protein expression but critical for intracellular Gag localization.
  • ZAP-70 in infected donor cells was required for efficient HIV transmission and virological synapse formation.

Conclusions:

  • ZAP-70 plays a vital role in late stages of HIV replication, specifically in viral assembly and cell-to-cell spread.
  • HIV appears to hijack components of the T-cell activation machinery, including ZAP-70, to facilitate its transmission through virological synapses.

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