Gamma-Delta T-Cell Phenotype and Function in DAA-Treated HIV-HCV Co-Infected and HCV-Mono-Infected Subjects

Area of Science:

• Immunology
• Hepatology
• Virology

Background:

• HIV-HCV co-infection increases liver fibrosis risk due to immune imbalances.
• Direct-acting antivirals (DAAs) are standard HCV treatment, but their immune effects in co-infected patients are unclear.
• Understanding immune cell dynamics is crucial for managing co-infection complications.

Purpose of the Study:

• To evaluate the impact of DAA treatment on immune cell populations in HIV-HCV co-infected individuals.
• To compare immune changes between HIV-HCV co-infected and HCV mono-infected patients post-DAA therapy.
• To investigate the relationship between immune alterations and liver health markers.

Main Methods:

• Assessed γδ T-cell phenotype and function, Treg and Th17 frequencies, γ-globulins, and B-cell activation.
• Studied 47 HIV-HCV co-infected and 35 HCV mono-infected individuals before and after DAA treatment (SVR12).
• Analyzed changes in immune markers and their correlation with liver enzymes and fibrosis indicators.

Main Results:

• DAA treatment reduced γδ T-cell activation and B-cell activation in both groups, with higher persistent activation in HIV-HCV co-infected individuals.
• The Vδ2/Th17 ratio increased significantly post-treatment in both groups, showing an inverse link to liver damage, particularly in co-infected patients.
• No significant changes were observed in γδ T-cell function or Treg frequencies; B-cell activation and γ-globulin levels remained elevated in co-infected subjects.

Conclusions:

• DAA therapy modulates specific immune cell subsets (γδ T-cells, B-cells) and the Vδ2/Th17 ratio in HIV-HCV co-infected and HCV mono-infected individuals.
• Persistent immune alterations in co-infected patients post-treatment may contribute to the risk of hepatic and extrahepatic complications.
• Further research is needed to understand the long-term implications of these immune changes for patient outcomes.