Human immunodeficiency virus type 1 Gag-derived peptides presented by major histocompatibility complex class I (HIV-1 Gag/MHC-I)

HIV-1 Gag-derived peptides presented by MHC class I molecules are critical targets for the cellular immune response against HIV-1. The Gag polyprotein is processed into several subunits, including p17 and p24, which are cleaved into short peptides and presented on the surface of infected cells by Major Histocompatibility Complex (MHC) class I molecules (Walker et al., 1987, Nature). These peptide-MHC (pMHC) complexes are recognized by the T-cell receptors (TCRs) of CD8+ cytotoxic T lymphocytes (CTLs), triggering the destruction of the infected cell (Goulder & Watkins, 2004, Nature Reviews Immunology). Because Gag is highly conserved and expressed early in the viral life cycle, it is a primary focus for the development of therapeutic vaccines and adoptive T-cell therapies, such as TCR-engineered T cells (Kan-Mitchell et al., 2004, Journal of Immunology). However, the high mutation rate of HIV-1 often leads to "viral escape," where mutations in the Gag sequence prevent MHC binding or TCR recognition, posing a significant challenge for sustained therapeutic efficacy (Borrow et al., 1997, Nature Medicine). Current clinical efforts involve engineering T cells with high-affinity TCRs to target stable epitopes like SL9 (SLYNTVATL) to achieve functional cures (Vasan et al., 2011, PLoS ONE).

Other names

HIV-1 Gag p24 peptidesHIV-1 Gag p17 peptidesGag-MHC-I complexesHLA-restricted HIV-1 Gag epitopesHIV-1 Gag SLYNTVATL (SL9) epitope

Recognition of the Gag peptide-MHC complex by endogenous or engineered T-cell receptors, leading to the activation of cytotoxic pathways and apoptosis of HIV-1 infected cells.