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Possible role of human interleukin‐6 and soluble interleukin‐6 receptor in hepatitis B virus infection
Author(s) -
Heinz D.,
Peters M.,
Prange R.,
Gerken G.,
RoseJohn S.
Publication year - 2001
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1046/j.1365-2893.2001.00281.x
Subject(s) - hepatitis b virus , receptor , recombinant dna , virology , alpha interferon , glycoprotein 130 , interleukin , virus , hepatitis b virus pre beta , interferon , immunology , biology , microbiology and biotechnology , medicine , interleukin 6 , cytokine , hepatitis b virus dna polymerase , biochemistry , gene
Human interleukin‐6 has been shown to promote hepatitis B virus (HBV) infection. However, it is not clear whether this influence is the result of a direct interaction between interleukin‐6 (IL‐6) and the HBV envelope proteins or of a rather indirect mechanism. A direct interaction of IL‐6 and the preS region of the large envelope protein ( L ‐protein) of HBV has been reported. In this study we assessed the binding of IL‐6 and of the IL‐6 receptor subunits to the preS region of the L ‐protein of HBV. Binding of IL‐6 and IL‐6 receptor subunits sIL‐6R and gp130 to preS was assessed by immunoprecipitation with recombinant preS proteins. In patient sera IL‐6 and sIL‐6R concentrations were analysed with respect to the course of hepatitis B infection during and after interferon‐α (IFN‐α) therapy. The IL‐6 and IL‐6 receptor subunits could not be precipitated with recombinant preS proteins. In sera of patients who responded to IFN‐α therapy by virus elimination, a significant increase in sIL‐6R concentration was measured. No increase in sIL‐6R levels was seen in patients who did not respond to IFN‐α. Hence, IL‐6 and IL‐6 receptor subunits do not bind to preS directly. A possible role for sIL‐6R in the elimination of HBV infection is discussed.