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By Dr. A. Vallbracht, B. Fleischer (auth.), Prof. Dr. C. De Bac, Dr. G. Taliani, Prof. Dr. W. H. Gerlich (eds.)

Chronic viral hepatitis is mentioned the following in a multidisciplinary method. The editors' target was once to gather contributions from clinicians, laboratory physicians, epidemiologists, pathologists, and molecular biologists to supply a synopsis of the entire very important points of this sickness. A key point within the continual evolution of viral hepatitis is the chronic coexistence of a cytotoxic immune reaction and viral gene expression that's mentioned in 11 articles on immune pathogenesis. The oncogenicity of hepatitis B virus on the molecular point and of hepatitis C virus on the epidemiological point is mentioned in chapters. the appliance of PCR for the detection of hepatitis viruses and their editions is an important subject of either sensible and theoretical curiosity. The scientific value of newly built serological assays for analysis and prevention is mentioned extensive via experts from clinics, transfusion facilities and virological laboratories. The remedy of persistent viral hepatitis continues to be unsatisfactory, yet a few gradual growth is defined in numerous articles. moreover, the quantity has a unique bankruptcy at the frequently missed subject of continual hepatitis in childhood.

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1), as previously reported in the mouse system [5]. In addition, more than one peptide fragment is usually recognized by T cells of individual patients (not shown). However, the most relevant finding of our study is the identification of an immunodominant amino acid sequence (residues 50-69) which was recognized by all but one patient (95%) (Fig. 1). Even though the detection of a significant response to native HBcAg was generally associated with the presence of a significant T cell response to peptide 50-69, in a minority of patients studied serially during the course of the disease, T cell recognition of peptide 50-69 was only transient and undetectable in a few time points when T cells were still able to recognize the native HBcAg and other core peptides.

In contrast, a spontaneous secretion of anti-HBc antibodies was registered in 2/10 B-cell cultures from HBsAg-CARRIER 300 HB-IMMUNE @] @J 200 E en 100 E zw 0 0 i= z <:! 1 1 10 1001ng/mll HEPATITIS B CORE ANTIGEN Fig. 1. Antigen dose dependency of HBcAg induced anti-HBc secretion. 001-100 ng/ml) ofHBcAg for 12 days. Anti-HBc secretion is given as ng/ml/l x 106 B-cells S. P. E. Sylvan et al. 4 It! :! ~ c. 2 v HBcAg ControlS + HBcAg + HBcAg Carriers Immune Fig. 2. Anti-HBc levels in supernatants ofT-cell depleted B-cell cultures from seven control individuals (_), eight HB-immune donors (e) and ten chronic HBsAg carriers (~) of whom three were HBV-DNA positive in serum (*) in the absence (open symbols) and presence (filled symbols) of optimal concentrations of HBcAg 1000 ~01 C ,....

Ferrari l ,2 I Cattedra Malattie Infettive, Universita di Parma, Parma, Italy 2 Department of Molecular and Experimental Medicine, Scripps Clinic and Research Foundation, LA Jolla, CA, USA Summary. The fine specificity of the human T cell response to the hepatitis B virus core antigen (HBcAg) was investigated in 23 patients with acute hepatitis B virus (HBV) infection using a panel of short synthetic peptides covering the entire core region. An immunodominant T cell epitope which was recognized by all except one patient, was identified within the core sequence 50-69.

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