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An antibody, which is distinct from the HBsAg- reacts with antigenic sites on Dane particles- HBcAg and HBeAg, was studied by radioimmunoprecipitation of radioactive intact hepatitis B virions in sera obtained early in the course of acute hepatitis type B. The antibody, previously termed anti-Dane particle (anti-DP) antibody, was reactive with Dane particles and HBsAg particles obtained from HBeAg-positive sera but not with HBsAg particles from anti-HBe containing sera. The expression on virus particles of the evoking antigen correlated with levels of binding sites for polymerized human serum albumin (pHSA) as detected by solid-phase radioimmunoassay. In acute hepatitis B sera, levels of anti-DP antibody activity showed inverse correlation with expression of pHSA receptors on circulating virus particles, although the two reactivities were not mutually exclusive. In inhibition experiments, pHSA blocked precipitation of Dane particles by anti-DP positive sera, while native human albumin and polymerized bovine albumin had no effect. The inhibition by pHSA of the anti-DP reaction appeared specific since identical concentrations of pHSA did not interfere with precipitation of virus particles by anti-HBs. Affinity chromatography studies with anti-DP insolubilized on Sepharose 4B columns showed selective binding to the gel of radioactive Dane particles; 125I-HBsAg was not reactive. The binding of Dane particles to anti-DP columns was completely inhibited when virus particles were applied to the gel in pHSA; pretreatment of the column with pHSA did not affect the reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatitis B virus markers were tested in the serum of 49 children with acute leukemia on clinical presentation and during subsequent chemotherapy. Hepatitis B surface antigenemia was observed in only six patients (12%), none of whom progressed to chronic infection. Chemotherapy had a marked suppressive effect on the production of antibodies to hepatitis B virus antigens and overt infection occurred in two children after suppression of protective immunity. Evidence of liver damage was frequently observed and was largely independent of serologic data. These results indicate that active immunization with hepatitis B vaccine may not find a clear place in this clinical setting.

In an assessment of the clinical relevance of serum hepatitis B virus (HBV) DNA testing in chronic HBV infection, changes in the presence of this marker were investigated by spot hybridization in 138 hepatitis B surface antigen (HBsAg)-positive patients with chronic liver disease who were followed up for one to eight years. Forty-one patients were treated with steroids, often with evidence of potentiation of viral replication, whereas 92 patients remained untreated and had no evidence of sigma agent infection during follow-up. Data analysis in these patients allowed us to determine the significance of testing for hepatitis B e antigen and for HBV DNA in the natural history of the infection. The findings indicate that sequential testing for serum HBV DNA may be of great importance in HBsAg chronic carriers with liver disease for adequate evaluation of HBV replication and for the contribution of HBV DNA to the clinical assessment of chronic hepatitis.

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