T-lymphocyte response to hepatitis C virus in different clinical courses of infection

Hepatitis C virus-specific reactivity of CD4+-lymphocytes in children born from HCV-infected women

“…On the contrary, in the mothers the proliferative responses to HCV-peptides were less frequent, restricted to a lower number of peptides, and the proliferation to the peptide derived from the core protein was less intense. These findings are in accordance with those reported in several cohorts of adults in different clinical stages of HCV infection, demonstrating impaired HCV-specific T-cell reactivity in chronically infected patients, and highlighting the protective role of T-cell responses to HCV structural proteins against the development of chronic hepatitis [16][17][18]. Notably, none of the three children with vertical HCV infection presented lymphocyte proliferation in response to peptides from core or envelope.…”

Enhancement of CD4 and CD8 immunity by anti-CD137 (4-1BB) monoclonal antibodies during hepatitis C vaccination with recombinant adenovirus

“…However, they are weak and inefficient [3][4][5][6][7][8][9][10]14,15,45]. In fact, the frequency of CTL precursors against HCV proteins found in patients with chronic hepatitis C is very low, in comparison to that found in HIV or CMV infections [46][47][48].…”

“…It is characterised by a high tendency to chronicity, which often progresses to cirrhosis and liver cancer [2]. Viral clearance after acute hepatitis or after IFN-␣ therapy is usually associated with strong CD4 and CD8 T cell responses [3][4][5][6][7][8][9][10][11][12]. In particular, cellular T helper immune response against nonstructural NS3 HCV protein has been associated with viral clearance after acute infection, whereas absence of this Tcell response leads to viral persistence and chronic hepatitis [9,13].…”

Influence of HLA haplotypes on the clinical courses of individuals infected with hepatitis C virus

“…6,7 In chronic HCV infection, HCV-specific CD4 ؉ or CD8 ؉ T-cell responses play essential roles in the pathogenesis of liver disease. [31][32][33] At the induction phase of these responses, activation signals are transduced to T cells in the context of the HLA-peptide-T-cell receptor complex. Thus, the variety of binding affinities of antigenic peptides to some HLA molecules might modify the degree of T-cell activation or T-cell anergy.…”