Scand J Gastroenterol 1995;30:609-613. REVIEW The exact mechanisms mediating the hepatocellular injury in the direct anti-viral action of interferon as measured by chronic hepatitis C virus (HCV) infection are still unknown. decreasing serum levels of viral DNA is evident, although Previous histologic findings in non-A, non-B hepatitis usually not accompanied by declining ALAT levels. Nor- (NANBH) and the rapid decrease in alanine aminotrans- malization of ALAT levels is not accomplished until after ferase (ALAT) levels after interferon treatment suggest a 3-4 months of treatment, when, in some patients, a bio- direct viral cytopathic injury, which contradicts the generally chemical reactivation with temporarily increased ALAT activity is followed by seroconversion to anti-HBe, dis- accepted idea of an immune-mediated liver injury in chronic hepatitis B. The purpose of this paper is to review the appearance of serum hepatitis B virus (HBV)-DNA, and normalization of ALAT (8). The preceding event is believed increasing clinical evidence that implicates immune- to be an interferon-induced enhancement of hepatocyte mediated mechanisms as also important in hepatitis C. human leucocyte antigen (HLA) class-I antigen expression, enabling sensitized cytotoxic T cells to attack the infected Findings suggestive of cytopathic viral effects hepatocytes (9). In comparison, hepatitis C patients who In general, the histologic findings are not pathognomonic respond to interferon therapy have a rapid and often com- for the different viruses causing chronic hepatitis or for plete normalization of ALAT levels (without a preceding autoimmune hepatitis. The histologic classification has peak), which is accompanied by a decrease or disappearance...