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Characterization of a novel binding site for the human immunodeficiency virus type 1 envelope protein gp120 on human

M Ma1, J D Geiger, A Nath

  • 1Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada.

Journal of Virology
|October 1, 1994
PubMed

Insights

Human fetal astrocytes bind to a specific site for the HIV-1 gp120 protein. This binding does not involve CD4 or galactocerebroside, suggesting a novel interaction pathway for HIV entry into astrocytes.

Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • The human immunodeficiency virus type 1 (HIV-1) can infect various cell types within the central nervous system, including astrocytes.
  • The gp120 envelope glycoprotein is crucial for HIV-1 entry into host cells, typically by binding to the CD4 receptor.

Purpose of the Study:

  • To investigate the binding characteristics of HIV-1 gp120 to primary human fetal astrocytes.
  • To determine the specific receptors or binding sites involved in this interaction.

Main Methods:

  • Primary cultures of human fetal astrocytes were utilized.
  • Binding assays were performed using 125I-labeled recombinant gp120.
  • Experiments included testing for the presence of CD4 and galactocerebroside, and blocking studies with specific antibodies.

Main Results:

  • 125I-labeled recombinant gp120 demonstrated binding to astrocytes, indicating a single class of 260-kDa binding sites.
  • The binding affinity (Kd) was determined to be 26 nM, with a maximal binding capacity of 29.9 fmol/4 x 10(4) cells.
  • Astrocytes lacked detectable CD4 and galactocerebroside; binding was not inhibited by antibodies against these molecules.

Conclusions:

  • Human fetal astrocytes possess specific binding sites for HIV-1 gp120, independent of CD4 or galactocerebroside.
  • These findings suggest a potential alternative mechanism for HIV-1 entry or interaction with astrocytes in the brain.
  • Further research is warranted to identify the precise nature of the 260-kDa binding site and its role in neuro-AIDS pathogenesis.

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