# The APPEESFRS Peptide, Restricted by the HLA-B*35:01 Molecule, and the APPEESFRF Variant Derived from an Autologous HIV-1 Strain Induces Polyfunctional Responses in CD8+ T Cells

## TL;DR

This study compares how two HIV peptides affect CD8+ T-cell responses, finding that one variant may enhance immune function and control HIV replication.

## Contribution

The study evaluates autologous HIV peptides' impact on CD8+ T-cell functionality, revealing insights into immune responses against circulating HIV strains.

## Key findings

- AF9 peptide elicited stronger CD8+ T-cell responses compared to AS9, though not statistically significant.
- AF9 induced a polyfunctional profile with cytokines like TNFα, IL-2, and MIP1β.
- Higher TNFα production in response to AF9 correlated negatively with HIV viral load.

## Abstract

Numerous reports have focused on consensus peptides to determine CD8+ T-cell responses; however, few studies evaluated the functional profile using peptides derived from circulating strains of a specific region. We determined the effector profile and maturation phenotype of CD8+ T-cells targeting the consensus APPEESFRS (AS9) epitope and its variant APPEESFRF (AF9), previously identified. The free energy of binding, maturation phenotype, and polyfunctional profile of both peptides were similar. The magnitude of CD8+ T-cell responses to AF9 was greater than the one elicited by AS9, although the difference was not significant. The polyfunctional profile of AF9 was characterized by CD107a/interleukin-2 (IL-2)/macrophage inflammatory protein beta (MIP1β) and by interferon gamma (IFNγ)/MIP1β/tumor necrosis factor alpha (TNFα) in response to AS9. TNFα production was significantly higher in response to AF9 than to AS9, and there was a negative correlation between the absolute number of CD8+ T-cell-producing TNFα and the plasma human immunodeficiency virus (HIV) load, suggesting a role of this cytokine in the control of HIV replication.