HIV-1 Intersection with CD4 T Cell Vesicle Exocytosis: Intercellular Communication Goes Viral

Helena Soares1

  • 1Instituto Gulbenkian de Ciência , Oeiras , Portugal ; Faculdade de Ciências Médicas, CEDOC, Universidade Nova de Lisboa , Lisboa , Portugal.

Frontiers in Immunology
|October 9, 2014
PubMed

Insights

CD4 T cell activation involves two exocytic events, including T cell receptor secretion. Human immunodeficiency virus-1 (HIV-1) exploits this process for viral budding and to induce bystander cell death, offering therapeutic targets.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Extracellular vesicle secretion in immune cells is modulated by cellular activation.
  • T cell activation occurs via cell-cell contact with antigen-presenting cells, forming an immunological synapse.
  • CD4 T cell activation involves two distinct exocytic events following T cell receptor (TCR) recognition.

Purpose of the Study:

  • To review the role of CD4 vesicle exocytosis in immune regulation.
  • To examine how HIV-1 hijacks CD4 T cell exocytosis for viral replication and pathogenesis.
  • To discuss potential therapeutic strategies targeting CD4 vesicle exocytosis.

Main Methods:

  • Review of existing literature on CD4 T cell activation and exocytosis.
  • Analysis of mechanisms by which HIV-1 interacts with the regulated secretory system of CD4 T cells.
  • Discussion of the implications of these processes for immune function and disease.

Main Results:

  • Cognate antigen recognition by the TCR triggers two exocytic events: signaling molecule targeting and TCR extracellular secretion.
  • HIV-1 co-opts the regulated secretory pathway of CD4 T cells for viral budding.
  • HIV-1-induced exocytosis contributes to bystander T cell death.

Conclusions:

  • CD4 vesicle exocytosis is crucial for T cell immune regulation and synapse formation.
  • HIV-1 pathogenesis is significantly linked to the manipulation of CD4 T cell exocytosis.
  • Targeting CD4 vesicle exocytosis presents a potential therapeutic avenue for HIV-1 infection.

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