Radioimmunoprecipitation Assay for Australia Antigen, Antibody, and Antigen-Antibody Complexes

1971 ◽  
Vol 138 (1) ◽  
pp. 249-257 ◽  
Author(s):  
J. A. Coller ◽  
I. Millman ◽  
T. C. Halbherr ◽  
B. S. Blumberg
Nature ◽  
1970 ◽  
Vol 226 (5240) ◽  
pp. 83-84 ◽  
Author(s):  
IRVING MILLMAN ◽  
W. THOMAS LONDON ◽  
ALTON I. SUTNICK ◽  
BARUCH S. BLUMBERG

The Lancet ◽  
1971 ◽  
Vol 298 (7718) ◽  
pp. 234-237 ◽  
Author(s):  
Burton Combes ◽  
James Shorey ◽  
Arnaldo Barrera ◽  
Peter Stastny ◽  
EdwinH. Eigenbrodt ◽  
...  

The Lancet ◽  
1971 ◽  
Vol 298 (7736) ◽  
pp. 1225-1227 ◽  
Author(s):  
JuneD Almeida ◽  
D Rubenstein ◽  
E.J Stott

PEDIATRICS ◽  
1974 ◽  
Vol 54 (2) ◽  
pp. 157-164
Author(s):  
Christos A. Kattamis ◽  
Demetrios Demetrios ◽  
Nicholas S. Matsaniotis

The status of Australia antigen (Au-Ag) and Australia antigen antibody (Au-Ab) was investigated in 27 infants less than 4 months of age with direct reacting hyperbilirubinemia, and in their parents. A diagnosis of viral hepatitis could be excluded in eight infants; of the remaining 19, ten were positive for Au-Ag and another three had suggestive evidence of hepatitis virus B (HBV) infection. The high proportion of infants with neonatal hepatitis associated with Au-Ag in this series is attributed to the high prevalence of Au-Ag carriers in Greece as well as to the high frequency of exchange transfusions in newborn infants. The other 14 cases of direct-reacting hyperbilirubinemia, none of which showed Au-Ag or evidence of HBV, were due to congenital malformation of the biliary tract (four cases), septicemia (three cases), cytomegalovirus (CMV) infection (one case), and fructosemia (one case). The remaining five patients, all of whom recovered, are believed to have hepatitis virus A infection. The detection of Au-Ag in prolonged neonatal jaundice with direct bilirubinemia favors a diagnosis of hepatitis type B, which in our experience carries a graver prognosis reflected in deaths and cirrhosis when compared to neonatal hepatitis not associated with Au-Ag. In our patients, it is inferred that transmission of Au-Ag to the infants occurred at or after birth, rather than during intrauterine life.


1971 ◽  
Vol 134 (3) ◽  
pp. 320-329 ◽  
Author(s):  
Baruch S. Blumberg ◽  
Irving Millman ◽  
Alton I. Sutnick ◽  
W. Thomas London

There is considerable data to support the hypothesis that Australia antigen is an infectious agent that causes hepatitis in man. (a) Association with acute viral hepatitis. (b) Association with chronic hepatitis. (c) Virus-like appearance under the electron microscope (200-A particles). (d) Transmission of Au(1) from man to man. (e) Transmission and passage of partially purified Au(1) to an animal host (infant African green monkey). (f) Localization [with fluorescent anti-Au(1)] of Au(1) in the nuclei of liver cells of patients with hepatitis and/or Au(1) in their blood. (g) Distribution of Au(1) in institutions, disease groups, and populations is consistent with the distribution of an infectious agent. (h) RNA identified in Au(1) particles isolated from blood. (i) Apparent replication of Australia antigen in tissue cultures of human liver cells. There is also considerable evidence that Australia antigen has many of the characteristics of a serum protein polymorphism. Since neither of these hypotheses has been rejected they can be combined to make a third hypothesis, namely, that Australia antigen is an infectious agent which causes hepatitis in some people infected with it and that it has the characteristics of an (inhertied) serum protein polymorphism. We propose calling agents of this postulated class "Icrons."


1971 ◽  
Vol 21 (6) ◽  
pp. 1017-1023
Author(s):  
V. J. Cabasso ◽  
R. Nieman ◽  
D. D. Schroeder ◽  
K. A. Hok ◽  
R. E. Louie ◽  
...  

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