The histopathology of hepatitis delta virus disease was studied in carriers of HBsAg with chronic hepatitis delta antigen-positive hepatitis and in serial biopsies of patients with acute hepatitis delta virus hepatitis that progressed to chronicity.
There was no histologic feature distinctive of hepatitis delta virus from other types of viral hepatitis. Biopsy specimens of patients with chronic disease exhibited portal and periportal inflammation with piecemeal necrosis, conforming to a picture of aggressive hepatitis often accompanied by cirrhosis. Characteristic was a marked intralobular infiltration by mononuclear cells and a degenerative eosinophilic change of the hepatocytic cytoplasms conducive to the formation of acidophilic bodies.
Liver specimens from patients with hepatitis delta virus hepatitis exhibited aspects of focal, confluent and bridging necrosis. The disease progressed to chronicity irrespective of the original histological features.
The expression of intrahepatic hepatitis delta antigen was reduced in the phase of the acute hepatitis but increased in parallel with the development of chronic active liver disease. In late-stage cirrhosis, expression of hepatitis delta antigen was usually low.
The discovery of the hepatitis delta virus (HDV) has led to the recognition that this defective pathogen, biologically dependent on the hepatitis B virus (HBV), may cause liver disease masking as hepatitis B. The HDV infection may complicate preexisting HBV hepatitis or induce new disease in previously healthy carriers (1).
Reports of the pathological aspects of chronic HDV hepatitis have been few, made difficult by the problem of distinguishing the aspects induced by this virus from those induced by the concomitant HBV infection. To determine the pathological features related to chronic HDV infection, we have in this study examined the liver histology of carriers of HBsAg who had intrahepatic HD antigen (HDAg) and an inactive type of HBV infection; they were considered examples of "pure" or predominant HDV disease on the assumption that the latent HBV