Hepatitis is caused by hepatitis viruses, but
hepatitis or hepatocellular
enzyme abnormalities is sometimes associated with
infection by the hepatiticomimetic viruses. The direct and indirect effects of
infection with hepatiticomimetic viruses were examined in two human hepatocyte systems. Poliovirus, adenovirus, and herpes simplex virus (HSV) induced cytopathology in Hep G2 cells. Measles virus caused no change in hepatocytes. Poliovirus
infection did not affect cellular
protein synthesis, and the peak of hepatocellular
enzyme release coincided with the peak of virus release. The increase in adenovirus
protein synthesis correlated with the decrease of
transferrin synthesis, and
enzyme release was not prominent. HSV induced
viral protein synthesis with enhanced processing and inhibition of synthesis of alpha1-antitrypsin. The peak of
enzyme release was later than the peak of virus release. In primary hepatocytes, poliovirus, adenovirus, and induced extensive cytopathology and
enzyme release, and VZV caused cytopathology and significant but minute
enzyme release. The ratio of
lactate dehydrogenase to
aspartate aminotransferase release was larger in poliovirus
infection in both hepatocytes than in HSV or VZV
infection. Although poliovirus and adenovirus are released by cytolysis and HSV and VZV are secreted by exocytosis of cytoplasmic vacuoles,
enzyme release was independent of the type of virus release. Adenovirus showed strong cytotoxicity but did not modify the membrane nor cause
enzyme release.
Enzyme release was associated with modification of the surface membrane due to apoptosis with poliovirus and
necrosis with HSV. Consequently hepatocellular injury by
viral infection did not reflect the amount or pattern of hepatocellular
enzyme release.