Anti-viral, hepatitis C virus (HCV)-specific immune T cell responses are functionally defective in patients with chronic hepatitis C and this functional impairment is believed to contribute to virus persistence. Persistent exposure to high virus loads is likely involved in the pathogenesis of T cell dysfunction. The underlying hypothesis of the project is that the level of anti-viral immune dysfunction in chronic HCV infection is a causal factor which can influence non-response to therapy. Although the rate of response to direct anti-viral agent (DAA) therapy, in untreated, non-cirrhotic, patients is between 95% and 100%, however, the response rate is lower in specific subgroups of patients, including genotype 3 cirrhotics and patients with decompensated cirrhosis, irrespective of the infecting genotype. Aim of the present study will be thus to understand whether non-response to therapy is associated with a wider and deeper anti-viral immune dysfunction, by comparing individual HCV-specific T cell responses in two groups of responder and non-responder patients. Characterization of protective immunity in non-responder patients could allow to identify baseline predictors of non-response to therapy to be used in the daily clinical practice. Objective of the study will be to compare the features (intensity and quality) of the overall HCV-specific immune T cell response in patients non-responder and responder to DAA therapy. To achieve this goal, T lymphocytes (either CD4 or CD8) isolated from the peripheral blood of the patients, before starting DAA therapy, will be stimulated with HCV proteins to evaluate the capacity of those cells to expand, produce cytokines and express cytotoxic capacity.
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Immune T cell response
Timeframe: between 12 and 14 months from the beginning of the study