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Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay
Published on: September 14, 2014
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The EBI2 receptor is coexpressed with CCR5 in CD4 + T cells and boosts HIV-1 R5 replication
Adeline Guigues1, Sandrine Gimenez1, Clément Mettling1
1Institut de Génétique Humaine, CNRS-Université de Montpellier UMR9002.
AIDS (London, England)
|May 21, 2024
Summary
Epstein-Barr virus-induced gene 2 (EBI2) enhances HIV-1 R5 infection in CD4+ T cells by promoting viral entry and replication. Targeting EBI2 may reduce persistent HIV replication in treated patients.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Most HIV strains utilize CCR5 as a coreceptor for entry into host cells.
- Identifying other host factors that modulate HIV-1 infection is crucial for therapeutic development.
Purpose of the Study:
- To investigate the role of other G protein-coupled receptors (GPCRs) in modulating HIV-1 infection.
- To analyze the effect of EBI2, when coexpressed with CCR5, on the HIV-1 replicative cycle.
Main Methods:
- Multi-RT-qPCR to identify GPCRs in primary CD4+ CCR5+ T cells.
- Förster resonance energy transfer (FRET) to study GPCR dimerization.
- Quantification of HIV-1 entry, transcription, and viral production using various assays (e.g., ELISA, qPCR, immunofluorescence).
Main Results:
- EBI2 is expressed in primary CD4+ CCR5+ T cells and heterodimerizes with CCR5.
- Coexpression of EBI2 and CCR5 reduced viral entry by 50% but increased HIV-1 R5 replication.
- EBI2 presence induced NF-kB translocation and activated HIV-1 genome expression, leading to significant R5 overproduction.
Conclusions:
- EBI2 expression in CD4+ CCR5+ cells boosts productive HIV-1 R5 infection.
- Constant EBI2 activation may enhance HIV replication in T cells due to its ligand presence.
- EBI2 antagonists could be explored to reduce residual viral production in treated patients.
