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An anti-CD4 (CDR3-loop) monoclonal antibody inhibits human immunodeficiency virus type 1 envelope

C Guillerm1, V Robert-Hebmann, U Hibner

  • 1Laboratoire Infections Rétrovirales et Signalisation Cellulaire, Institut de Biologie, CRBM/CNRS UPR 1086, 4 Boulevard Henri IV, Montpellier Cedex, 34060, France.

Virology
|August 29, 1998
PubMed

Insights

An anti-CD4 antibody, 13B8.2, prevents human immunodeficiency virus type 1 (HIV-1) induced cell death by targeting specific CD4 epitopes. This antibody inhibits viral replication and protects cells from HIV-1 mediated programmed cell death.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Programmed cell death (PCD) is a critical cellular process.
  • Human immunodeficiency virus type 1 (HIV-1) infection can induce PCD in host cells.
  • Anti-CD4 monoclonal antibodies (mAbs) are being investigated for their therapeutic potential.

Purpose of the Study:

  • To investigate the role of anti-CD4 mAbs in inhibiting HIV-1-induced PCD.
  • To identify specific CD4 epitopes involved in protection against HIV-1-induced PCD.
  • To elucidate the mechanisms by which anti-CD4 mAbs confer protection.

Main Methods:

  • Utilized the DNA intercalant YOPRO-1 assay to measure PCD.
  • Tested the efficacy of anti-CD4 mAbs 13B8.2 and BL4 in protecting HIV-1 infected cell cultures.
  • Investigated the effect of 13B8.2 mAb on syncytia formation, virus transcription, and PCD mediated by viral envelope glycoproteins.

Main Results:

  • The anti-CD4 mAb 13B8.2 protected infected CEM cell cultures against HIV-1-induced PCD.
  • Another anti-CD4 mAb, BL4, did not provide protection, indicating the importance of specific CD4 epitope engagement.
  • 13B8.2 mAb inhibited HIV-1 replication, virus spread, and PCD mediated by membrane-expressed HIV-1 envelope glycoproteins.
  • 13B8.2 mAb did not interfere with PCD induced by Fas, dexamethasone, or serum withdrawal.

Conclusions:

  • Specific engagement of CD4 epitopes by mAbs like 13B8.2 can inhibit HIV-1-induced PCD.
  • 13B8.2 mAb likely protects cells by inhibiting viral replication, preventing viral envelope-CD4 interactions, and/or interfering with apoptotic signaling pathways.
  • 13B8.2 mAb represents a potential therapeutic strategy for mitigating HIV-1-induced cellular damage.

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