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Actin-dependent receptor colocalization required for human immunodeficiency virus entry into host cells

S Iyengar1, J E Hildreth, D H Schwartz

  • 1Department of Pharmacology and Molecular Sciences, School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205, USA.

Journal of Virology
|May 30, 1998
PubMed

Insights

Human immunodeficiency virus (HIV) entry into cells depends on coreceptor concentration, which is actin-dependent. Disrupting this process with cytochalasin D (CytoD) blocks viral entry and infection without harming cells.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Human immunodeficiency virus (HIV) envelope proteins mediate viral entry by binding to CD4 and chemokine receptors.
  • This sequential binding facilitates the release of viral gp41, inserting into the target cell membrane.

Purpose of the Study:

  • To investigate the role of actin-dependent coreceptor clustering in HIV entry.
  • To determine the effect of cytochalasin D (CytoD) on HIV coreceptor dynamics and viral infection.

Main Methods:

  • Utilized immunofluorescent confocal microscopy to visualize CD4 and CXCR4 distribution on activated peripheral blood mononuclear cells (PBMCs).
  • Assessed the impact of cytochalasin D (CytoD) on coreceptor clustering, pseudopod formation, and HIV entry and infection.
  • Investigated the effect of CytoD pretreatment on PBMCs versus the virus itself.

Main Results:

  • HIV entry was found to be dependent on the actin-dependent concentration of coreceptors (CD4 and CXCR4).
  • CytoD disrupted this coreceptor clustering and subsequent pseudopod formation, completely blocking viral membrane changes.
  • Pretreatment of PBMCs, but not the virus, with CytoD inhibited HIV entry and infection, without affecting cell viability or mitosis.

Conclusions:

  • Actin-dependent clustering of CD4 and chemokine receptors is essential for efficient HIV entry.
  • Targeting the actin cytoskeleton or coreceptor dynamics presents a potential strategy for inhibiting HIV infection.

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