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Updated: Jul 10, 2026

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
07:22

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion

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An intercellular adhesion molecule-3 (ICAM-3) -grabbing nonintegrin (DC-SIGN) efficiently blocks HIV viral budding

Qiuwei Wang1, Shen Pang

  • 1UCLA School of Dentistry, 10833 Le Conte Ave., Los Angeles, CA 90095, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 27, 2007
PubMed

Insights

Dendritic cell-specific intercellular adhesion molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) and DC-SIGNR effectively inhibit HIV budding. These proteins block viral production by reducing cell surface gp120 and stripping it from virions.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • HIV life cycle inhibition is well-studied except for assembly and budding stages.
  • Targeting HIV assembly and budding presents a novel therapeutic strategy.

Purpose of the Study:

  • To investigate the role of DC-SIGN and DC-SIGNR in inhibiting HIV assembly and budding.
  • To determine the mechanism by which DC-SIGN and DC-SIGNR affect HIV production.

Main Methods:

  • Cotransfection of DC-SIGN or DC-SIGNR with HIV in host cells.
  • Quantification of viral production and gp120 levels on cell membranes and virions.

Main Results:

  • DC-SIGN and DC-SIGNR demonstrated significant inhibition of HIV budding (95-99.5%).
  • These proteins reduced HIV generation by 90-95%.
  • DC-SIGN reduced cell surface gp120 and completely stripped gp120 from produced virions.

Conclusions:

  • DC-SIGN and DC-SIGNR are effective inhibitors of HIV assembly and budding.
  • The mechanism involves gp120 internalization mediated by DC-SIGN.
  • This finding opens new avenues for HIV therapeutic interventions targeting viral egress.

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