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Sustained virological response to peginterferon plus ribavirin in chronic hepatitis C genotype 1 patients is associated with a persistent Th1 immune response
Author(s) -
TRAPEROMARUGÁN M.,
GARCÍABUEY L.,
MUÑOZ C.,
QUINTA. E.,
MORENOMONTEAGUDO J. A.,
BORQUE M. J.,
FERNÁNDEZ M. J.,
SALVANÉS F. R.,
MEDINA J.,
MORENOOTERO R.
Publication year - 2006
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2006.02954.x
Subject(s) - ribavirin , medicine , immune system , cd8 , immunology , hepatitis c virus , flow cytometry , cytokine , hepatitis c , interferon , gastroenterology , virus
Summary Background An impairment of cellular immune response may contribute to the persistency of hepatitis C virus infection. Aim To analyse the Th1/Th2 cytokine profile in peripheral blood CD4+ and CD8+ T cells from patients with chronic hepatitis C (CHC) during treatment with pegylated interferon‐ α 2a plus ribavirin and to correlate the Th1/Th2 balance with virological response (SVR). Methods Prospective longitudinal study: 44 naïve genotype 1 CHC patients received PEG‐IFN α 2a plus ribavirin for 48 weeks: 26 (59.1%) achieved a SVR, 13 relapsed (29.5%) and 5 (11.4%) were non‐responders. Sixteen healthy controls were analysed. The production of IL‐4, IFN γ and TNF α by CD4+ and CD8+ T cells was measured using flow cytometry, both in resting and phorbol‐ester‐stimulated cells. Results First three months of treatment: the synthesis of TNF α by phorbol‐ester‐stimulated‐CD4+ T cells was higher in patients with SVR ( P < 0.01). At the end of treatment, SVR was associated with higher intracellular expression of IFN γ by stimulated‐CD4+ and CD8+ T cells ( P < 0.05). At the end of follow‐up, a higher intracellular expression of IFN γ by CD4+ T cells was associated with a SVR. Conclusions A Th1‐type immune response was associated with achievement of a SVR, as indicated by the persistent elevation of intracellular IFN γ and TNF α .