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Functionally distinct T-Cell epitopes within the hepatitis C virus non-structural 3 protein

1999; Elsevier BV; Volume: 60; Issue: 2 Linguagem: Inglês

10.1016/s0198-8859(98)00102-5

1879-1166

Niloofar M. Tabatabai, Tong-hua Bian, Charles M. Rice, Kaname Yoshizawa, Joan Cox Gill, David D. Eckels,

Viral Infections and Immunology Research

Clearance of Hepatitis C Virus (HCV) infection is an uncommon phenomenon. To understand the mechanism of viral persistence despite active cellular and humoral responses, we examined the in vitro cytokine response of PBMC from an HCV sero-positive, asymptomatic individual to recombinant intact antigen and sixty-nine overlapping peptides of the HCV non-structural (NS) 3 protein. Whereas, intact antigen induced strong proliferation and significant levels of γIFN and IL-10, little or no IL-2 was produced. Only 7% of peptides induced IL-2, which also coincided with their ability to stimulate proliferation. In contrast, 38% of the peptides induced γIFN while 35% induced IL-10. All IL-2 stimulating peptides also induced significant levels of γIFN and among these, a peptide corresponding to residues 358–375 was the strongest. In addition, 16% of the peptides induced both γIFN and IL-10. Exogenous recombinant IL-10 inhibited proliferation and IL-2 induction in response to peptide 358–375. Furthermore, neutralization of IL-10 with an anti–IL-10 antibody resulted in enhanced IL-2 production in response to recombinant NS3 protein. We suggest that IL-10 inducing epitopes within HCV NS3 may thus down-regulate IL-2 dependent T-cell responses.