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T‐ and B‐cell responses to different hepatitis C virus antigens in patients with chronic hepatitis C infection and in healthy anti‐ hepatitis C virus—positive blood donors without viremi
Author(s) -
Lechmann M,
Ihlenfeldt H G,
Braunschweiger I,
Giers G,
Jung G,
Matz B,
Kaiser R,
Sauerbruch T,
Spengler U
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510240406
Subject(s) - hepatitis c virus , ns5a , immunology , ns5b , antigen , antibody , virology , lymphoproliferative response , immune system , epitope , ns3 , hepatitis c , virus , medicine , t cell , hepacivirus , biology , peripheral blood mononuclear cell , biochemistry , in vitro
As the host's immune response may determine the course of hepatitis C virus (HCV) infection, we studied the humoral and cellular immune responses to HCV‐related antigens in subjects with different outcomes of HCV infection. Lymphoproliferative responses and circulating antibodies to a panel of HCV core‐ and E1‐related 25‐mer peptides were examined in 10 healthy anti‐HCV‐seropositive blood donors (group A) and in 29 patients with chronic hepatitis C (group B). In addition, cellular recognition of recombinant HCV proteins (core, NS3, NS4A, NS5A, NS5B) were investigated. In group A, stronger T‐cell responses were detected against both HCV proteins (core, P = .03; NS4, P = .005; NS5B, P = .03) and peptides. Proliferation was induced by the same peptides in each group, defining at least five distinctive epitopes within core (amino acids [aa] of 20‐44, aa 39‐63, aa 79‐103, aa 118‐152 and aa 148‐172) and three regions within E1(aa 198‐252, aa 308‐372, and aa 368‐392). Subjects with strong T‐cell responses had low or no detectable levels of peptide‐specific antibodies, and vice versa. In particular, T‐cell responses were more common in group A; B‐cell responses were more common in group B. From our data, we conclude that a benign course of HCV infection may be the consequence of the effective activation of T‐helper lymphocytes.