Chemokine Receptor 5 Has No Major Role in the Severity of Hepatitis C Virus-Related Liver Damage

Giuseppe Colucci, Roberta D'Ambrosio, Enrico Galmozzi, Marco Maggioni, Stella De Nicola, Alessio Aghemo, Massimo Colombo

Research output: Contribution to journalArticle

Abstract

Total or partial inactivation of the chemokine 5 (CC5) pathway, as caused by the CC5 receptor Δ32 deletion (CCR5Δ32), may result in a profound manipulation of immune surveillance with significant consequences on the course and response to therapy of diverse human infections, including HIV. It has been postulated that in chronic hepatitis C (CHC), such a deregulation of CC5 pathway may compromise T cell-dependent antiviral immune responses, which in turn may favor viral persistence. To test this hypothesis, we investigated a cohort of 100 patients with CHC in whom 12 heterozygous and 1 homozygous CCR5Δ32 mutations were detected compared to 8 and none in 98 healthy controls (13% vs. 8.2%, p = 0.36). As patients with and without CCR5Δ32 mutations were similar in terms of histological activity (p = 0.84) and fibrosis stage (p = 0.20) as well as CCR5 tissue expression, we reasonably exclude that this CCR5 mutation is significantly involved in the pathogenesis of CHC and may be a potential therapeutic target. However, deleted patients showed a significantly higher response to pegylated interferon-alfa (PEG-IFN), suggesting that a dormant immune system is more readily primed by immunostimulation.

Original languageEnglish
Pages (from-to)358-361
Number of pages4
JournalViral Immunology
Volume31
Issue number5
DOIs
Publication statusPublished - Jun 1 2018

    Fingerprint

Keywords

  • CCR5
  • CCR5D32
  • Chronic hepatitis C
  • histological grade
  • histological stage

ASJC Scopus subject areas

  • Immunology
  • Molecular Medicine
  • Virology

Cite this