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Immunoglobulin M (IgM) antibodies against hepatitis B core antigen (anti-HBc) and hepatitis A virus (anti-HAV) were determined in 41 cases of acute viral hepatitis. In sera positive for anti-HBc or anti-HAV, IgM was separated from IgG by reorienting sucrose gradient high-speed centrifugation, and the IgG- and IgM-containing serum fractions were tested for the presence of specific antibody by radioimmunoassay. At the onset of illness, 4 of the 41 cases were classified as hepatitis A, 31 were hepatitis B, and 6 were non-A, non-B hepatitis, based on the results of these tests and of assays for hepatitis B surface antigen and antibody and hepatitis B e antigen and antibody. Fourteen of these 41 patients (34%) required IgM anti-HBc or IgM anti-HAV testing or both for appropriate classification. IgM anti-HBc persisted for at least 7 weeks after onset but no longer than 17 weeks in all patients tested with transient hepatitis B surface antigen-positive acute hepatitis. IgM anti-HAV persisted up to but not longer than 62 days in the patients with hepatitis A. Therefore, IgM anti-HBc and IgM anti-HAV determinants are valuable tools for the differential diagnosis of acute A, B, and non-A, non-B hepatitis.

Liver biopsies from five patients with chronic non-A, non-B (NANB) hepatitis were examined by electron microscopy for hepatocellular alterations. Circular fused membranes were observed within the cytoplasm of hepatocytes of four of the patients. Aggregates of intranuclear particles, measuring 22 +/- 2 nm in diameter, were also seen in two of the biopsies in which fused membranes were identified. Sera of all five patients formed precipitin lines detectable by counterimmunoelectrophoresis when reacted with serum from an individual convalescent from posttransfusion NANB hepatitis. Using this convalescent serum as an antibody source, complexes of 22 +/- 2 nm particles were identified in three of the chronic patient sera by immunoelectron microscopy. These observations suggest that at last one of the agents responsible for NANB hepatitis elicits both nuclear and cytoplasmic modifications. Furthermore, the 22 +/- 2 nm particles circulating in the sera of the chronic NANB patients may represent components related to NANB hepatitis agent.

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