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Updated: Jun 12, 2026

Isolation, Transfection, and Culture of Primary Human Monocytes
09:13

Isolation, Transfection, and Culture of Primary Human Monocytes

Published on: December 16, 2019

Transcriptome analysis of monocyte-HIV interactions.

Rafael Van den Bergh1, Eric Florence, Erika Vlieghe

  • 1Department of Molecular and Cellular Interactions, VIB, Brussels, Belgium. rvdbergh@vub.ac.be

Retrovirology
|June 16, 2010
PubMed
Summary
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HIV infection causes monocyte dysfunction, impacting pathogenesis. Antiretroviral therapy (ART) partially restores gene expression, but novel factors like NAMPT/visfatin may inhibit HIV, offering new therapeutic avenues.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Monocytes and macrophages are crucial in HIV pathogenesis and complications.
  • Dysfunctions in these cells during HIV infection and antiretroviral therapy (ART) are significant but poorly understood at a molecular level.

Purpose of the Study:

  • To characterize molecular components contributing to monocyte dysfunction in HIV infection and/or ART.
  • To identify novel genes and pathways involved in HIV pathogenesis and ART-associated disorders.

Main Methods:

  • Parallel approach using genome-wide microarray analysis and focused gene expression profiling.
  • Analysis of monocytes from patients at different stages of HIV infection and/or ART.

Main Results:

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Last Updated: Jun 12, 2026

Isolation, Transfection, and Culture of Primary Human Monocytes
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Published on: December 16, 2019

An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells
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An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells

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  • Identified monocyte dysfunctions in apoptosis, cell cycle, lipid metabolism, proteasome function, protein trafficking, and transcriptional regulation.
  • Discovered NAMPT/visfatin as a potential inhibitor of HIV replication.
  • Observed partial restoration of gene expression under ART, with some persistent dysregulation.
  • Suggested CCL1 and CYP2C19 as candidate biomarkers for abacavir hypersensitivity.

Conclusions:

  • Confirmed known and identified novel areas of monocyte dysfunction in HIV infection.
  • Pinpointed specific genes contributing to HIV-related monocyte dysfunctions and ART complications.
  • Highlighted NAMPT/visfatin as a potential novel HIV restriction factor, warranting further functional studies.