Abstract

Approximately 25% of HIV-infected patients are co-infected with HCV. Notably, the burden of HCV infection (e.g., viral persistence, viral load, or HCV-related liver symptoms) is more pronounced in the presence of HIV co-infection. However, to date, the underlying immune mechanisms accounting for accelerated disease progression in HIV/HCV-coinfected individuals have not been described in sufficient detail. We hypothesized that regulatory T cells (Treg) bearing potent immunosuppressive capacities could not only play a substantial role in the pathogenesis of HCV/HIV coinfection but also modulate the response to the standard anti-viral therapy. Materials and Methods: To this end, we studied alterations in frequencies of Treg cells in correlation with other Treg-related and virus-related parameters in both HCV and HCV/HIV-infected patients subjected to standard pegIFN-α/RBV therapy. Results: Notably, we found that pegIFN-α/RBV therapy significantly increased levels of Treg cells in HCV-infected but not in HIV/HCV-coinfected individuals. Furthermore, HIV/HCV-coinfection was demonstrated to inhibit expansion of regulatory T cells during anti-viral treatment; thus, it might probably be responsible for viral persistence and HCV-related liver damage. Conclusions: Therapy with pegIFN-α/RBV demonstrated a significant effect on regulatory T cells in the course of HIV and/or HCV infection indicating a crucial role in the anti-viral immune response.

Highlights

  • Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection affect approximately 25% of HIV-infected individuals

  • No significant differences were observed in routine laboratory tests results between the control group, HCV-infected, and HCV/HIV-coinfected cohorts prior to pegIFN-α/RBVbased treatment

  • HCV-infected patients were clinically stable with no critical changes in, inter alia, liver function-related parameters, with only a slight increase in serum alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT)

Read more

Summary

Introduction

Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection affect approximately 25% of HIV-infected individuals. Clinical evidence has shown a higher rate of HCV viral persistence and increased viral load in HCV/HIV-coinfected patients compared to subjects with HCV monoinfection [2]. HIV infection is associated with higher HCV RNA viral load and more rapid progression of HCV-associated liver diseases [3,4,5]. Mechanisms of accelerated disease progression in HIV/HCV-coinfection have not been fully determined. Disturbances in virus-specific T cell responses via altered activity of regulatory T cells (Treg ) are thought to play an important role [6,7,8] in infections caused by HIV, HCV, and herpes virus [9,10,11,12].

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call