Scientific publications

Production of interleukin-2 in response to synthetic peptides from hepatitis C virus E1 protein in patients with chronic hepatitis C: relationship with the response to interferon treatment

Sarobe P, Jauregui JI, Lasarte JJ, García N [SP], Civeira MP [SP], Borrás-Cuesta F, Prieto J.
Department of Medicine, University of Navarra, Pamplona, Spain

Magazine: Journal of Hepatology

Date: Jul 1, 1996


The role of cellular immunity in the clearance of hepatitis C virus after interferon therapy has not yet been elucidated. Here, we analyzed the T cell response to peptides from hepatitis C virus E1 protein in untreated and interferon-treated patients with chronic hepatitis C virus infection.

We used thirty-six 15-mer synthetic peptides from hepatitis C virus E1 protein (genotype 1a) in a sensitive interleukin-2 production assay in two groups of controls (healthy seronegative individuals and patients with liver diseases unrelated to hepatitis C virus), and three groups of patients with chronic hepatitis C: nine patients who cleared the virus after interferon treatment (group 1), nine patients who failed to respond to the therapy (group 2) and nine previously untreated patients (group 3).

None of the controls responded to any of the peptides tested, whereas 8/9 (88%) of patients from group 1 responded positively. In contrast, only 2/9 (22%) of patients from group 2 showed peptide recognition. In group 3, 5/9 patients (55%) displayed positive response against E1 peptides. When E1 peptides from the sequence corresponding to genotype 1b (the commonest in patients who were non-responders to interferon) were tested in nine additional interferon-resistant patients (group 2*) a positive response was detected in only three of them (33%).

T cell recognition of hepatitis C virus E1 peptides in patients with chronic hepatitis C who exhibit sustained response to interferon therapy is increased as compared with interferon-resistant cases, suggesting that T cell immunity to hepatitis C virus structural proteins may play a role in the clearance of this viral infection.

CITATION  J Hepatol. 1996 Jul;25(1):1-9

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