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The potential significance of adaptive evolution and dimerization in chimpanzee intercellular cell adhesion molecules

Nicole A R Walter1, Justin Stebbing, Walter Messier

  • 1Evolutionary Genomics, Colorado Bioscience Park Center, 12635 East Montview Boulevard, Aurora, Colorado 80010, USA. waltern@ohsu.edu

Journal of Theoretical Biology
|December 2, 2004
PubMed

Insights

Chimpanzee intercellular cell adhesion molecules (ICAMs) show adaptive evolution, potentially explaining their resistance to immunodeficiency virus progression. This suggests ICAMs evolved to control viral binding and infection.

Area of Science:

  • Evolutionary biology
  • Immunology
  • Virology

Background:

  • Cell adhesion molecules (ICAMs) play roles in cellular processes.
  • Human immunodeficiency virus (HIV-1) hijacks ICAM functions to boost infection.
  • Chimpanzees infected with immunodeficiency viruses often do not progress to disease.

Purpose of the Study:

  • Investigate adaptive changes in chimpanzee ICAMs and their ligands.
  • Understand the mechanisms behind non-progression in SIVcpz-infected chimpanzees.

Main Methods:

  • Amplified protein coding regions of non-human primate ICAMs 1-5 and ligands LFA-1/Mac-1.
  • Utilized phylogenetic tree-based comparative genomics to detect adaptive evolution.
  • Screened for Darwinian positive selection in ICAM genes.

Main Results:

  • Observed strong positive selection in chimpanzee ICAMs 1, 2, and 3.
  • Identified selection hotspots in ICAM-1 dimerization domains.
  • Hypothesized evolved ICAM dimerization modulates ligand binding, including virion attachment.

Conclusions:

  • Chimpanzee ICAMs exhibit adaptive evolution potentially linked to viral resistance.
  • Evolved ICAM dimerization may explain lack of immunosuppression in HIV-1/SIVcpz-infected chimpanzees.
  • Ancient retroviral pandemics may have driven chimpanzee ICAM adaptation.

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