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A new antigen antibody system the e Ag and Ab has been investigated by immunodiffusion and counterelectrophoresis in the serum of 509 subjects. Those included 242 patients with polyarteritis, acute chronic or fulminant hepatitis; 85 hemodialysis HBs Ag carriers and 182 asymptomatic HBs Ag carrier blood donors. Neither e Ag nor anti- e were detected in any of the non hepatitis B virus associated cases. Counterelectrophoresis was found to be more sensitive than immunodiffusion and detected either e Ag or anti- e in 24 p. cent more cases. e Ag was found among HBs Ag positive patients with polyarteritis, chronic hepatitis or under going hemodialysis. Anti- e was observed in 28 p. cent to 66 p. cent of asymptomatic HBs Ag carriers. The study of the nature and prognostic significance of e Ag and anti- e appear of major importance in the understanding and follow up of HB virus infections.

Using immunodiffusion, a major cross-reactivity had been previously demonstrated between hepatitis B(HBe/3 Ag) and the antigen reported in the serum on non A, non-B hepatitis patients, therefore redesignated NANBe Ag. By direct immunofluorescence a new antigen associated with, but distinct from, NANBe Ag has now been identified in the liver of 14/26 patients with NANB chronic active hepatitis. The homologous antibody was detected in the serum of these 14 patients. Behaving like HBc Ag and cross reacting with it by immunofluorescence, the new antigen was termed NANBc Ag. Anti NANBc also became detectable in serial acute phase and convalescence sera from 5/5 NANB Ag-positive posttransfusion hepatitis cases. Further characterization of NANBe and NANBc antigens achieved by fractionation of a NANB virus-infected liver showed NANBc Ag to be expressed on 22-25 nm HB core-like particles containing DNA polymerase activity. Cross-reactivity between NANBc and HBc antigens was confirmed by immunodiffusion. Liver-derived NANBe Ag identical to serum NANBe Ag exhibited the same physical properties as HBe/3 Ag and could be similarly released by disruption of the non-A, non-B, virus cores. These results indicate that hepatitis B and NANB virions not only share the same structure and DNA polymerase activity but are also antigenically related and belong to the same new class of DNA viruses.

Two hepatocellular carcinomas, induced in woodchucks chronically infected with woodchuck hepatitis virus, were characterized for viral integration near c-myc and alterations of c-myc expression. In one tumor, viral integration within the untranslated region of c-myc exon 3 resulted in overexpression of a long c-myc viral cotranscript. In the second tumor, a single insertion of highly rearranged viral sequences 600 bp upstream of c-myc exon 1 was associated with increased levels of normal c-myc mRNA. In both cases, viral enhancer insertion and disruption of normal c-myc transcriptional or posttranscriptional control appear to be involved in c-myc activation. These results demonstrate that integration of woodchuck hepatitis virus near a cellular proto-oncogene, as in several retroviral models, can contribute to the genesis of liver tumors.

In-frame and frameshift mutations were introduced into the pre-S region (1,212 base pairs) of duck hepatitis B virus. The in-frame mutants retained the inserted 12 nucleotides, while the frameshift mutants either reverted to wild type or exhibited a 10-nucleotide compensatory deletion downstream of the original mutation site. Thus, although duck hepatitis B virus has a compact and highly economical genome organization, it can replicate despite alterations of up to 9 amino acid codons in the pre-S and P open reading frames.

The purpose of this work was to study the hemodynamic effects of a pituitary extract (Post-Hypophyse, Choay, EPH) and of lysine vasopressin (Diapid, Sandoz, VP). Cardiac, pulmonary and liver hemodynamics were measured in 50 cirrhotic patients before and during intravenous infusion (0.45 IU/kg/h) of EPH (24 patients) or VP (26 patients). EPH and VP did not have identical consequences in cardiac output and systemic resistances. EPH significantly increased cardiac output and significantly decreased systemic resistances while VP significantly and increased systemic resistances. Both vasoactive drugs similarly decreased myocardial performances. EPH and VP had a moderate influence on WHV/IVC pressure gradient. This was variable from one patient to another. The decrease of WHV/IVC pressure gradient observed during EPH infusion was mainly related to an increase of IVC pressure. Since the effects of both drugs on WHV/IVC pressure gradient are slight and unpredictable and they exert an important effect on cardiopulmonary hemodynamics, caution should be taken in administering EPH or VP to cirrhotic patients. The clinical use of EPH or VP should be undertaken only when cardiac and liver hemodynamics monitoring are available.

Clinical expression and outcome of hepatis B virus infections associated with human immunodeficiency virus infection (without AIDS) were studied in 17 homosexuals during 23 months. In an attempt to distinguish the respective impacts of homosexuality from that of human immuno-deficiency virus, patient were compared with a population of homosexual males infected by hepatitis B virus alone. The ratio of biochemical evidence of liver cell necrosis (ALAT)/viral replication (DNAp) was significatively decreased (p less than 0.01), despite evidence of severe histological damage in some cases. Two-thirds of patients with HBV replication tolerated HBV infection at the end of follow-up. This tolerance was significatively more common than in homosexuals infected by HBV alone (p less than 0.01), and did not appear to be related to decreased T4 cell count but seemed to correlate with the existence of the AIDS related complex.