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Related Experiment Videos

Restricted entry of R5 HIV Type 1 strains into eosinophilic cells.

R J Taylor1, D Schols, D P Wooley

  • 1Biomedical Sciences Ph.D. Program, Wright State University, Dayton, Ohio 45435, USA.

AIDS Research and Human Retroviruses
|December 14, 2004
PubMed
Summary

T cell-tropic HIV-1 (X4) infects eosinophils via CXCR4, while macrophage-tropic HIV-1 (R5) cannot enter these cells. This finding is crucial for understanding AIDS pathogenesis, especially in later infection stages.

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Previous studies showed T cell-tropic HIV-1 (CXCR4-using) infects eosinophils, unlike macrophage-tropic HIV-1 (CCR5-using).
  • Eosinophils play a role in immune responses and their susceptibility to HIV-1 is an area of interest.

Purpose of the Study:

  • To refine the understanding of HIV-1 tropism and coreceptor usage in eosinophilic cells.
  • To investigate viral entry and restriction levels in an improved eosinophil cell culture model.

Main Methods:

  • Utilized an engineered AML14.3D10-CCR3 cell line expressing CD4, CXCR4, CCR5, and CCR3 to mimic primary eosinophils.
  • Employed PCR to detect early reverse transcription products, indicating viral entry.
  • Conducted coreceptor blocking experiments using AMD3100 (CXCR4 antagonist).

Related Experiment Videos

  • Measured virus production using p24 immunoassay.

    • Main Results:

    • T cell-tropic (X4) HIV-1 successfully entered and replicated in engineered eosinophilic cells, leading to decreased cell viability.
    • Macrophage-tropic (R5) HIV-1, despite CCR3 expression, failed to enter eosinophilic cells.
    • AMD3100 completely blocked X4 HIV-1 infection, confirming exclusive CXCR4 usage.

    Conclusions:

    • Eosinophils are susceptible to X4 HIV-1 infection, mediated solely by the CXCR4 coreceptor.
    • R5 HIV-1 strains are restricted from entering eosinophilic cells, even with CCR3 present.
    • The susceptibility of eosinophils to X4 HIV-1 has significant implications for AIDS pathogenesis, particularly during late-stage infection when X4 strains are prevalent.