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Hepatitis B virus‐specific T cell response in chronic hepatitis B patients treated with lamivudine and interferon‐α
Author(s) -
Pontesilli Oscar,
Van Nunen Andeltje B.,
Van Riel Debby,
Carotenuto Patrizia,
Niesters Hubert G.,
Uytdehaag Fons G.,
De Man Robert A.,
Osterhaus Albert D.
Publication year - 2004
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2004.0922.x
Subject(s) - lamivudine , medicine , hbcag , immunology , hepatitis b virus , discontinuation , interferon , immune system , hepatitis b , virus , viral load , combination therapy , virology , lymphoproliferative response , hbsag , biology , peripheral blood mononuclear cell , biochemistry , in vitro
Aims: The goal of the present study was to assess the impact combination antiviral therapy has on immune responses in chronic hepatitis B. Materials and methods: T cell responses were studied in 16 chronically hepatitis B virus (HBV)‐infected patients treated with sequential, partially overlapping, lamivudine‐interferon (IFN)‐α combination therapy. Results: HBcAg‐specific lymphoproliferative response (LPR) was transiently detected in four of five patients who achieved virus suppression (HBV DNA <10 4 genome equivalents/ml) at end of dual therapy, and then reverted to pre‐treatment viral load after therapy discontinuation. In contrast, no significant HBcAg‐specific LPR was detected in 8 patients who did not attain profound HBV suppression, as well as in three patients who experienced no HBV DNA rebound after therapy discontinuation. Conclusions: This pilot study suggests that restored viral replication after pharmacological suppression drives the immune response to HBV in chronically infected patients. Further characterization of the adaptive immunity and its regulatory mechanisms at time of therapy discontinuation appears therefore necessary in controlled trials.