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Updated: Aug 12, 2026

Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
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Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.

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Interleukin-16 inhibits human immunodeficiency virus type 1 entry and replication in macrophages and in dendritic

M J Truong1, E C Darcissac, E Hermann

  • 1Institut Pasteur de Lille, INSERM U167, 59019 Lille Cedex, France.

Journal of Virology
|July 10, 1999
PubMed

Insights

Recombinant interleukin-16 (rIL-16) effectively suppresses human immunodeficiency virus type 1 (HIV-1) replication in antigen-presenting cells (APCs). This cytokine blocks viral entry and reduces proviral DNA, showing potential for HIV treatment.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Recombinant interleukin-16 (rIL-16) inhibits HIV-1 replication in CD4(+) T cells.
  • The impact of rIL-16 on HIV-1 replication in antigen-presenting cells (APCs) remains uncharacterized.

Purpose of the Study:

  • To investigate the effect of rIL-16 on HIV-1 replication in APCs.
  • To determine the mechanism of rIL-16's anti-HIV activity in macrophages and dendritic cells.

Main Methods:

  • Assessed HIV-1 replication in monocyte-derived macrophages and dendritic cells treated with rIL-16.
  • Measured viral RNA transcripts and reverse transcriptase levels.
  • Evaluated the effect of rIL-16 timing and its impact on viral entry and proviral DNA.

Main Results:

  • rIL-16 demonstrated potent HIV-1 suppression in acutely infected APCs.
  • The suppressive effect required early rIL-16 exposure post-infection.
  • rIL-16 blocked HIV-1 entry and reduced proviral DNA in APCs without affecting beta-chemokines or enhancing cytokines.

Conclusions:

  • rIL-16 plays a critical role in protecting APCs from HIV-1 infection.
  • These findings support the potential therapeutic application of rIL-16 for HIV disease treatment.

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