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Miriam J. Alter, PhD

JAMA. 1996;276(10):845-846.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

DURING most of the 20th century, the study of viral hepatitis was dependent on observations of naturally occurring disease, usually in the form of epidemics, and of experimentally infected human volunteers, because of the failure both to isolate hepatitis virus in tissue culture and to identify a suitable animal model for transmission studies. These observations initially provided indirect evidence of 2 distinct forms of viral hepatitis; short-incubation infectious hepatitis and long-incubation serum hepatitis. These 2 forms were further shown to be immunologically distinct types of hepatitis that were designated as MS-1 (infectious) and MS-2 (serum).¹

The discovery of Australia antigen by Blumberg and colleagues in 1965² and its subsequent detection in blood donors and transfusion recipients with long-incubation clinical hepatitis suggested an association between this antigen and serum hepatitis. It was also demonstrated that the MS-2 serum was positive for this antigen, as were recipients who had been . . . [Full Text PDF of this Article]

Author Affiliations
From the Hepatitis Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Ga.

Footnotes
Reprints: Miriam J. Alter, PhD, Hepatitis Branch, Mailstop G37, Centers for Disease Control and Prevention, Atlanta, GA 30333.

A commentary on Barker LF, Shulman R, Murray R, et al. Transmission of serum hepatitis. JAMA. 1970;211:1509-1512.

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