Priming persistence of HCV.

Anita Schuch,Robert Thimme,Maike Hofmann

doi:10.18632/oncotarget.5445

Abstract

Priming persistence of HCV.

Highlights

Exhausted hepatitis C virus (HCV)-specific CD8+ T-cells are characterized by impaired effector functions and the coexpression of inhibitory receptors such as PD-1, 2B4 and KLRG1 (Figure.1)
HCV-specific CD8+ T-cells that target epitopes that underwent viral escape mutations express fewer inhibitory receptors and are marked by CD127 expression [1] (Figure 1). The identification of these distinct CD8+ T-cell phenotypes as markers for different mechanisms of CD8+ T-cell failure was based on analyses performed in patients with HCV-specific CD8+ T-cell populations that were detectable directly ex vivo by conventional peptide/MHC multimer staining
HCVspecific CD8+ T-cells were present in all chronically HCVinfected patients. These results indicate that the absence of virus-specific CD8+ T-cells does not contribute to HCV persistence in this cohort

Summary

Introduction

Acute infection with hepatitis C virus (HCV) is cleared in about 30% of cases with CD8+ T-cells being the main effector cells in viral elimination. Chronic HCV infection is characterized by an impaired virus-specific CD8+ T-cell response caused by several viral and host factors. Viral escape and CD8+ T-cell exhaustion due to prolonged antigen exposure, for example, cause impaired virus-specific CD8+ T-cell responses and contribute to HCV persistence.

Results

Conclusion