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Article
July 15, 1974

Viral Hepatitis: Light at the End of the Tunnel

Author Affiliations

Bethesda, Md
From the Blood Bank Department, Clinical Center, National Institutes of Health (Drs. Alter and Holland), and the Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (Dr. Purcell), Bethesda, Md.

JAMA. 1974;229(3):293-294. doi:10.1001/jama.1974.03230410017014
Abstract

AFTER decades of investigative frustration, it now appears that the viruses causing both type A and B hepatitis have been identified, that clear-cut serologic distinctions between these infectious agents have been demonstrated, and that a practical basis for a type B hepatitis vaccine has been established. These events have derived from the explosive proliferation of hepatitis research that followed the first description of the Australia antigen in 1965 by Blumberg et al.1 This commentary will not deal with the many important early discoveries in this area that have been extensively reviewed,2,3 but will focus on more recent findings that provide an experimental framework for our emerging concept of the agents responsible for viral hepatitis.

The Dane Particle  In addition to its clinical association with viral hepatitis, the Australia antigen, hereafter referred to as the hepatitis B surface antigen (HBsAg), became a candidate for the elusive type

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