Abstract
Peptide T is currently in phase II clinical trials for the treatment of AIDS-associated dementia. Its putative mode of action is inhibition of binding of the HIV envelope protein (gp120) to its cellular receptor (CD4), thus preventing viral infectivity and gp120-induced neuronal toxicity. However, a number of reports have appeared in the literature which have failed to observe any inhibitory activity of Peptide T on CD4-gp120 binding, thus casting doubt on this hypothesis. This study uses a novel biosensor technique to demonstrate that Peptide T does bind to CD4 and that this binding can be specifically inhibited by an anti-CD4 monoclonal antibody. A detailed analysis of the kinetics of the interaction is presented.
Original language | English |
---|---|
Pages (from-to) | 217-222 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 333 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1 Nov 1993 |
Externally published | Yes |
Keywords
- AIDS-associated dementia
- Biosensor
- Kinetics
- Peptide T
- Surface plasmon resonance