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From the Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06510; and the Connecticut Red Cross Blood Program of the American National Red Cross, Farmington, Connecticut 06032
Abstract
In the early days of testing for hepatitis B surface antigen (HB8Ag)2 and the homologous antibody (anti-HB8), there were reports of antigen and antibody co-existing in the same serum specimen (1, 2). Their subspecificities were not determined; but their homotypic character was evidently inferred, and in keeping with this idea were certain results obtained by complement fixation (3), and electronmicroscopic observations of circulating complexes apparently made up of HB8Ag-positive Australia particles and antibody molecules (4). Some recent studies have adduced further evidence for the existence of such complexes (5), whereas others have failed to substantiate the concurrent presence of HB8Ag and homologous anti-HB8, at least in the blood of asymptomatic carriers of the antigen (6).
With the definition of distinct antigenic phenotypes of HB8Ag, there arose the theoretical possibility that Australia particles of one phenotype might co-circulate with free anti-HB8 antibody directed against antigenic configurations characteristic of a different phenotype.
Footnotes
1 This work was supported by the United States Army Medical Research and Development Command (Contract No. DADA 17-70-C-0042), and by National Institutes of Health Biomedical Research Support Grant No. 5-S07-RR05443.
2 Abbreviations used in this paper: HB8Ag, hepatitis B surface antigen; anti-HB8, antibody against HB8Ag; HBV, hepatitis B virus; ID, immunodiffusion; RPHA, reversed passive hemagglutination; SGOT, serum glutamic oxalacetic transaminase.
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