For example, signaling of the inhibitory receptor PD-1 following binding to its ligand PD-L1 induces T-cell exhaustion, and blocking this pathway during chronic LCMV infection restores virus-specific CD8+ T-cell responses by inducing proliferation and cytokine secretion and reduction of viral load.23–25 Furthermore, blockade of the PD-1 pathway during chronic simian immunodeficiency virus infection induces rapid expansion of virus-specific CD8+ T cells with enhanced effector function resulting in improved survival.26 This evidence concerns the gene PDCD1 and simian immunodeficiency virus infection.