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Updated: May 5, 2026

Assessment of Immunologically Relevant Dynamic Tertiary Structural Features of the HIV-1 V3 Loop Crown R2 Sequence by ab initio Folding
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Assessment of Immunologically Relevant Dynamic Tertiary Structural Features of the HIV-1 V3 Loop Crown R2 Sequence by ab initio Folding

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A CD4 domain important for HIV-mediated syncytium formation lies outside the virus binding site

D Camerini1, B Seed

  • 1Department of Genetics, Harvard Medical School, Boston, Massachusetts.

Cell
|March 9, 1990
PubMed

Insights

Human CD4 protein differences explain why chimpanzees resist AIDS. Specific residue 87 in CD4 is key for cell fusion, impacting human immunodeficiency virus (HIV) spread and disease progression in different species.

Area of Science:

  • Virology
  • Immunology
  • Primatology

Background:

  • Human immunodeficiency virus (HIV) causes fatal immunodeficiency in humans but only chronic viremia in chimpanzees.
  • The CD4 receptor is crucial for HIV entry into host cells.

Purpose of the Study:

  • To investigate the molecular basis for the differential susceptibility of human versus chimpanzee cells to HIV-induced syncytia formation and viral entry.
  • To identify specific regions of the CD4 protein that regulate cell-to-cell fusion mediated by HIV envelope proteins.

Main Methods:

  • Comparative analysis of human, chimpanzee, and macaque CD4 protein sequences.
  • Functional assays measuring syncytia formation between cells expressing different CD4 variants and HIV envelope proteins.
  • Assessment of viral entry mechanisms, including sensitivity to lysosomotropic agents.

Main Results:

  • HIV envelope proteins mediate syncytia formation with human CD4 but not chimpanzee or macaque CD4.
  • A single amino acid substitution at residue 87 of chimpanzee CD4 with a human residue restores syncytia formation.
  • Viral entry into human cells expressing chimpanzee CD4 does not appear to require endocytosis.

Conclusions:

  • The differential course of HIV infection in humans and chimpanzees may be due to variations in the CD4 protein, specifically residue 87, affecting cell-to-cell transmission.
  • These findings highlight the importance of CD4-mediated cell fusion in HIV pathogenesis and suggest alternative viral entry pathways in certain host contexts.

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