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Publication : Genetic control of the murine humoral response to distinct epitopes of hepatitis C virus core protein.

First Author  Chen Z Year  1995
Journal  J Viral Hepat Volume  2
Issue  1 Pages  9-17
PubMed ID  7493296 Mgi Jnum  J:31390
Mgi Id  MGI:78891 Doi  10.1111/j.1365-2893.1995.tb00067.x
Citation  Chen Z, et al. (1995) Genetic control of the murine humoral response to distinct epitopes of hepatitis C virus core protein. J Viral Hepat 2(1):9-17
abstractText  Recombinant hepatitis C virus (HCV) core protein from aa1-164, designated cp1-10, was used to immunize mice. Antibodies to cp1-10 were produced in all seven strains of congenic mice; none of the strains could be considered low responders relative to the others. The mouse response against individual epitopes of HCV core protein varied from one strain to another: B10.RIII (H-2r) recognized all three peptides aa13-30, aa77-90, aa129-145; B10.D2 (H-2d), B10 (H-2b) and C3H.SW (H-2b) responded to aa13-30, aa77-90; B10.M (H-2f), B10.BR (H-2k) and C3H/Hej (H-2k) reacted with aa13-30 only. Competitive inhibition of binding demonstrated that antibody to the peptide was inhibited by cp1-10 protein and the corresponding peptide only. Recombinant HCV core protein is highly immunogenic and can elicit good antibody response in mice. The aa13-30 is a major epitope of HCV core protein in mice. The humoral response to the distinct epitopes was regulated by the H-2 genes. Further analysis indicated that the I-a locus of H-2 genes determined the antibody response to aa13-30 and 77-90. These results suggest that the variation of antibody responses to HCV in humans may partially contribute to different outcomes of HCV infection.
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