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Peripheral‐blood mononuclear cell responses to recombinant hepatitis C virus antigens in patients with chronic hepatitis C
Author(s) -
Schupper Haim,
Hayashi Paul,
Scheffel James,
Acettuno Sherri,
Paglieroni Teresa,
Holland Paul V.,
Zeldis Jerome B.
Publication year - 1993
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.1840180507
Subject(s) - peripheral blood mononuclear cell , virology , hepatitis c virus , antigen , antibody , virus , hepatitis b virus , immunology , hepatitis , biology , medicine , in vitro , biochemistry
Peripheral blood mononuclear cell proliferative responses in vitro to recombinant yeast or Escherichia coli hepatitis C virus fusion proteins were evaluated in 20 patients with chronic hepatitis C who were reactive for antibody to hepatitis C virus (on enzyme immunoassay, version 2.0, and a four‐antigen recombinant immunoblot assay). Twenty age‐matched, healthy individuals negative for antibody to hepatitis C virus were used as a control group. Peripheral‐blood mononuclear cells from all chronic hepatitis C patients with antibodies to hepatitis C virus antigens c22 and c100‐3 proliferated in vitro in response to the corresponding recombinant hepatitis C virus fusion protein. Peripheral‐blood mononuclear cells from 75% of patients infected with hepatitis C virus proliferated in response to cytidine monophosphate‐keto‐3‐deoxyoctulosonic acid–core recombinant antigen but there was no proliferative response to cytidine monophosphate‐keto‐3‐deoxyoctulosonic acid–EF (derived from the NS5 region). All hepatitis C virus–infected patients had 33c antibody, but peripheral‐blood mononuclear cells from only 9 of 14 (64%) proliferated in vitro in response to 33c. Ninety‐five percent of all hepatitis C virus–in‐fected patients had peripheral‐blood mononuclear cells that proliferated in response to at least one recombinant hepatitis C virus fusion protein. The numbers and percentages of CD3 T cells, CD19 B cells and natural killer cells from patients with chronic hepatitis C virus infection did not differ from those in the healthy control group. However, the number of non‐major histocompatibility complex–restricted cytotoxic T cells (CD3‐positive, CD56‐positive, CD16‐positive) was increased in patients with chronic hepatitis C virus infection (p < 0.05). (HEPATOLOGY 1993;18:1055‐1060).