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Updated: Sep 27, 2026

Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay
07:10

Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay

Published on: September 14, 2014

Human CD38 interferes with HIV-1 fusion through a sequence homologous to the V3 loop of the viral envelope

Andrea Savarino1, Thea Bensi, Annalisa Chiocchetti

  • 1Laboratory of Immunology, Interdisciplinary Research Center of Autoimmune Diseases, Department of Medical Science, University of Eastern Piedmont, Novara, Italy. asavarino@medscape.com

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|January 29, 2003
PubMed

Insights

CD38 protein inhibits HIV-1 entry by blocking the binding of viral gp120 to CD4 receptors. This anti-HIV activity is linked to a specific region of CD38 that mimics the HIV-1 V3 loop.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • CD38 is a known progression marker in HIV-1 infection.
  • CD38 associates with CD4 and modulates gp120/CD4 binding, impacting HIV-1 entry.

Purpose of the Study:

  • To elucidate the mechanism of interaction between CD4, CD38, and HIV-1.
  • To identify the specific region of CD38 responsible for its anti-HIV activity.

Main Methods:

  • Utilized mouse and human cell transfectants expressing CD4 and CD38 variants.
  • Employed bioinformatic analysis to map anti-HIV activity and assess sequence similarity.
  • Synthesized peptides derived from CD38 to test anti-HIV effects.

Main Results:

  • CD38 specifically inhibits gp120/CD4 binding, blocking HIV-1 entry.
  • The anti-HIV activity is concentrated in CD38's membrane-proximal region, which shares sequence similarity with the HIV-1 gp120 V3 loop.
  • Peptides mimicking this CD38 region effectively inhibited HIV-1 and HIV-2 replication.

Conclusions:

  • CD38's anti-HIV activity is mediated by a V3 loop-like region, offering insights into early HIV-1 fusion events.
  • This mechanism provides a potential new strategy for developing anti-HIV interventions.

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