Both serum IL-7 and CD127 expression on CD8<sup>+</sup> T cells was significantly reduced in chronic HCV-infected patients, which was negatively correlated with HCV RNA.
After antigen re-challenge the less differentiated TCF1<sup>+</sup>CD127<sup>+</sup>PD1<sup>+</sup> population expands, which is accompanied by emergence of terminally exhausted TCF1-CD127-PD1<sup>hi</sup> HCV-specific CD8<sup>+</sup> T cells.
Interestingly, CD127 expression on CD56<sup>bright</sup> NK cells negatively correlated with HCV plasma levels in HCV monoinfection and HCV-HIV coinfection.
The aim of this study was to examine the association of interleukin-7 receptor-α (IL7RA) polymorphisms with a sustained virologic response (SVR) after hepatitis C virus (HCV) therapy with pegylated interferon-alpha plus ribavirin (pegIFNα/ribavirin) in 177 human immunodeficiency virus (HIV)/HCV-coinfected patients.
Furthermore, HCV-infected patients with fibrosis presented with a higher proportion of CD4⁺ T cells expressing CD127 compared with HCV-infected patients without fibrosis [88.4% (84.5-91.0) versus 83.8% (79.9-86.8), P = 0.016].
Our data indicate that most CD8 T-cell responses in chronic HCV infection do not target the circulating virus and that the appearance of HCV-specific CD127(+) T cells is driven by viral variation.
In contrast, HCV-specific CD8(+) T cells in acute infections evolving to chronicity expressed low levels of CD127 and Bcl-2, exhibited diminished proliferation and cytokine production, and eventually disappeared from the periphery.