Table 1.
Summary of HIV-1 epitopes and naturally occurring APL
| Peptide epitope | Peptide Seq | HLA | Phenotype |
|---|---|---|---|
| HIV-1 17-3 Gag (Index) | GGKKKYKL | B8 | Agonist |
| HIV-1 17-3 Gag (7R) | GGKKKYRL | B8 | Agonist/Antag. |
| HIV-1 17-3 Gag (7Q) | GGKKKYQL | B8 | Agonist/Antag. |
| HIV-1 17-3 Gag (7A) | GGKKKYAL | B8 | Untested |
| HIV-1 17-8 Gag (Index) | SLYNTVATL | A2 | Agonist |
| HIV-1 17-8 Gag (3C) | SLCNTVATL | A2 | Agonist/Antag. |
| HIV-1 17-8 Gag (3S) | SLSNTVATL | A2 | Agonist/Antag. |
| HIV-1 17-8 Gag (3F, 6I, 8V) | SLFNTIAVL | A2 | Agonist/Antag. |
| HIV-1 17-8 Gag (3F, 5A) | SLFNAVATL | A2 | Strict antag. |
CTL lines were grown from patients’ peripheral blood mononuclear cells against the index peptides. Proviral sequence from patients mounting an HLA B8 p17-3 Gag (11) or HLA A2 p17-8 Gag (19) response revealed several codon-changing mutations within these epitopes. The effect of naturally ocurring APL on CTL-mediated lysis in response to index peptide was evaluated in chromium release killing assays. Partial agonists/antagonists (Agonist/Antag.) are defined as peptides that at low concentrations (<10−7 M; ref. 19) inhibit CTL-mediated lysis in response to agonist peptide, but at higher concentrations (>10−6 M) elicit lysis against themselves. Strict antagonists are defined as peptides that inhibit CTL-mediated lysis in response to agonist peptide but do not elicit lysis against themselves at any concentration measured (18). Underlined letters indicate MHC anchor residues; letters in boldface indicate variant amino acid.