The search for human hepatitis virus.
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Biomedical subjects
Publications and source records attributed to F Deinhardt.
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Inoculation of human serums or plasmas obtained during the early acute phase of viral hepatitis induced chemical and morphological hepatic disease in marmosets in two out of five experimental series. The disease was transmissible in series from marmoset to marmoset with an apparent increased virulence of the causative agent in later marmoset passages. The chemical evidence for the disease was elevation of the activity of SGOT and SICD and of serum bilirubin. In serial liver biopsy specimens interpreted under code, a hepatitis, exhibiting some of the characteristics of human viral hepatitis, was readily distinguishable from nonspecific changes. The morphological changes preceded the biochemical alterations and persisted after them. The data reported in these studies indicate that marmosets may be susceptible to human hepatitis. If these observations are confirmed, these animals may provide good experimental models for this disease. Final proof that the hepatitis observed in marmosets is caused by agents of human viral hepatitis is still lacking.
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By routine screening for serologic markers of hepatitis A and B in patients with acute hepatitis, 30 chronic carriers of hepatitis B virus with serologic evidence of acute hepatitis A and two patients with simultaneous acute infection with hepatitis A virus and hepatitis B virus were detected. For evaluation of clinical data, two major risk groups were distinguished. Nine patients were drug addicts and 17 were children and young adults from Mediterranean countries or southeast Asia. During the acute phase of illness, serum bilirubin and SGPT levels did not differ from those in other patients with acute hepatitis A. In three patients for whom follow-up sera were available, HBsAg concentration decreased during the acute stage of hepatitis A.
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