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Testing for e antigen and antibody (anti-e) was performed by immunodiffusion and counterelectrophoresis in patients with polyarteritis nodosa fulminant hepatitis, and chronic active hepatitis (CAH), in 59 asymptomatic carriers of hepatitis B surface antigen (HBsAg) who underwent liver biopsy, and in 150 carriers followed with sequential SGPT determinations. Counterelectrophoresis was more sensitive that immunodiffusion. Neither e antigen nor anti-e was found in the absence of HBsAg. Among HCsAg-positive patients with polyarteritis nodosa and CAH, e antigen was found in 16 of 18 and 13 of 22, respectively. It was not found in any of 43 patients with fulminant hepatitis, of whom 24 were HBsAg-positive. The e antigen was detected in none of 13 biopsied carriers with normal histology, 4 of 28 with nonspecific changes of 11 of 18 with CAH or chronic persistent hepatitis. Conversely, anti-e was present in 9 of 13 with normal biopsy, 7 of 28 with nonspecific changes, and none of 18 with CAH or chronic persistent hepatitis. The e antigen was found more commonly in nonbiopsied carriers with elevated SGPT, and anti-e in those with normal SGPT. Six carriers whose antigenemia terminated spontaneously had anti-e. The presence of e antigen correlated with a high titer of HBsAg, and with immunofluorescent detection of hepatitis B core antigen in the nuclei of hepatocytes. Conversely, anti-e was associated with significantly lower titers of serum HBsAg (P less than 0.001) and lack of detectable hepatitis B core antigen in the liver.

Hepatitis B surface antigen (HBSAg) and antibodies to both the surface and core antigens of the hepatitis B virus (anti-HBS and anti-HBC) have been studied in 64 consecutive cases of fulminant hepatitis. HBSAg was detected by counterelectrophoresis in 23 (35-9%) but by radioimmunoassay in 38 (59-3%). Anti-HBS was detected by passive haemagglutination in 26 (40-6%), coexisting HBSAg and anti-HBS were found in 16 cases (25%). Using an indirect immunofluorescence technique, anti-HBC was found in all of the cases in whom either HBSAg or anti-HBS was present. The highest survival rate was observed in patients with no evidence of HBV infection (31-3%) and was lowest in those who had both HBSAg and anti-HBS detected simultaneously (6-2%). The prognosis of those who exhibited anti-HBS only was no better than those with HBSAg alone. In a further case, transient interruption of the asymptomatic chronic HBSAg carrier state with seroconversion to anti-HBS was associated with the development of a fulminant hepatitis syndrome. The results suggest that an unusually strong and rapid immune clearance of HBSAg may be involved in the pathogenesis of fulminant hepatitis.

To investigate further the role of hepatitis B antigen (HBs Ag) and specific immune complexes in polyarteritis, sera from 55 histologically confirmed cases were tested for the presence of hepatitis B antigen-associated particles and hepatitis B-antibody (anti HBs) by solid phase radio-immunoassay, electron microscopy, and passive haemagglutination. Results of these findings have been correlated with the clinical course of the disease.HBs Ag was detected in 30 patients (54.5%) and anti HBs in 13/45 (28%). Subtyping in 20 patients revealed that 11 were Y and 9 D. Thirty-seven cases (69%) demonstrated either HBs Ag or anti HBs and 5/45 (11%) had both. Electron microscopic examination showed 20 nm spherical and tubular particles in sera of 20/27 patients with 42 nm particles in 11 cases and clumped particles in 12 (60%). No correlation was found between detection of immune complexes and liver disease whereas the presence of coexisting hepatitis B antigen and antibody or aggregated particles was restricted to cases of active vasculitis. Seroconversion or the presence of hepatitis B antibody alone was associated with improved prognosis. Circulating hepatitis B antigen antibody complexes may be responsible for vasculitis or polyarteritis but do not appear to be pathogenic for the liver.

Evidence from prospective studies of human cases of posttransfusion hepatitis observed among 299 cardiac surgery patients, and from each of three experimentally challenged chimpanzees, indicates that immunity to hepatitis B infection can be overcome by massive challenge doses. However, all cases of hepatitis in patients with prior immunity have been subclinical. Chimpanzees developed hepatitis and HBs antigenemia when challenged with hepatitis B virus that had an antigenic subtype identical to that used in the primary infection. This response provides evidence against the role of differences in antigenic composition of initial and challenge strains of virus as an explanation for incomplete homologous immunity.