Hepatitis E virus ORF 1 induces proliferative and functional T-cell responses in patients with ongoing and resolved hepatitis E

Liver Int. 2018 Feb;38(2):266-277. doi: 10.1111/liv.13521. Epub 2017 Aug 20.

Abstract

Background and aims: Hepatitis E virus (HEV) is a major cause of acute viral hepatitis with >3 million symptomatic cases per year accounting for 70 000 HEV-related deaths. HEV-specific T-cell responses have been investigated against structural proteins expressed by open reading frames (ORF) 2 and 3. T-cell responses against non-structural HEV proteins encoded by ORF1 are hardly studied. The aim of this study was to determine HEV ORF1-specific T-cell responses in comparison to ORF2/3 in patients exposed to HEV.

Methods: HEV-specific CD4+ and CD8+ T-cell responses against HEV genotype 3 were investigated in patients with acute and chronic hepatitis E as well as in HEV seropositive and seronegative individuals. HEV-specific T-cell responses were determined by proliferation and intracellular cytokine assay upon stimulation of PBMCs with HEV-specific overlapping peptide pools spanning the entire HEV genome. HEV-antigen was measured using an anti-HEV antigen-specific ELISA.

Results: Broad HEV ORF1-specific T-cell responses were detected in patients with acute, resolved and chronic hepatitis E without distinct dominant regions. The magnitude and frequency in recognition of ORF1-specific T-cell responses were similar compared to responses against HEV ORF2/3. Longitudinal studies of HEV-specific T-cell responses displayed similar behaviour against structural and non-structural proteins. HEV-antigen levels were inversely correlated with HEV-specific T-cell responses.

Conclusions: HEV-specific T-cell responses are detectable against the entire HEV genome including the non-structural proteins. HEV-specific T-cell responses are associated with control of HEV infection. These findings have implications for the design of HEV vaccines.

Keywords: HEV; HEV-antigen; ORF-1 response; hepatitis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adolescent
  • Adult
  • Aged
  • Cell Proliferation*
  • Cells, Cultured
  • Cytokines / immunology
  • Cytokines / metabolism
  • Female
  • Genotype
  • Hepatitis E / diagnosis
  • Hepatitis E / immunology*
  • Hepatitis E / virology
  • Hepatitis E virus / genetics
  • Hepatitis E virus / immunology*
  • Hepatitis E virus / metabolism
  • Hepatitis, Autoimmune / diagnosis
  • Hepatitis, Autoimmune / immunology*
  • Hepatitis, Autoimmune / metabolism
  • Hepatitis, Autoimmune / virology
  • Host-Pathogen Interactions
  • Humans
  • Lymphocyte Activation*
  • Male
  • Middle Aged
  • Open Reading Frames*
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / virology
  • Viral Proteins / genetics
  • Viral Proteins / immunology*
  • Viral Proteins / metabolism

Substances

  • Cytokines
  • Viral Proteins