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Intercellular adhesion molecule 3, a candidate human immunodeficiency virus type 1 co-receptor on lymphoid and

M A Sommerfelt1, B Asjö

  • 1Centre for Research in Virology, University of Bergen, Bergen High Technology Centre, Norway.

The Journal of General Virology
|June 1, 1995
PubMed

Insights

Researchers investigated how HIV enters cells, finding that Intercellular Adhesion Molecule 3 (ICAM-3) plays a key role in viral entry. Antibodies targeting ICAM-3 blocked HIV entry, suggesting it

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • CD4 is the primary receptor for human and simian immunodeficiency viruses (HIV and SIV).
  • HIV entry requires co-receptors beyond CD4 to mediate viral and cellular membrane fusion.
  • Adhesion molecules are potential candidates for HIV co-receptor function.

Purpose of the Study:

  • To identify candidate co-receptor molecules involved in HIV-1 entry.
  • To investigate the role of adhesion molecules in HIV-1-induced cell fusion and viral entry.

Main Methods:

  • Utilized a panel of monoclonal antibodies (MAbs) targeting adhesion molecules.
  • Assessed the inhibitory effects of MAbs on HIV-1-induced syncytium formation (cell fusion).
  • Evaluated the inhibitory effects of MAbs on HIV-1 entry into human SupT1 cells.

Main Results:

  • Antibodies against CD18, CD11b, and CD11c inhibited HIV-1-induced syncytium formation but not entry.
  • Certain antibodies against Intercellular Adhesion Molecule 3 (ICAM-3) significantly inhibited HIV-1 entry but not syncytium formation.
  • One MAb targeting ICAM-3 inhibited HIV-1-induced syncytium formation, entry, and infectivity.

Conclusions:

  • ICAM-3 is implicated as a co-receptor mediating HIV-1 entry into lymphoid and monocytoid cells.
  • Specific epitopes of ICAM-3 are crucial for HIV-1-specific entry.
  • Findings provide insights into the molecular mechanisms of HIV-1 cell entry.

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