In this study we have examined the localization of interferon-α in liver tissue from acute and chronic hepatitis B virus carriers to establish whether the defect in interferon-α production reported in chronic hepatitis B virus infection is at a pretranscriptional or posttranscriptional level using in situ hybridization and immunohistochemical techniques. Interferon-α messenger RNA transcripts and the immunoreactive protein were abundant in liver tissue and in particular in hepatocytes from patients with acute hepatitis B virus infection who ubsequently recovered. In contrast interferon-α polypeptide was present in a significantly lower number of sinusoidal cells, mononuclear cells and hepatocytes in chronic hepatitis B virus carriers. Although a high proportion of patients with chronic hepatitis B virus infection had cells that expressed interferon-α messenger RNA transcripts, the number of such cells was significantly less than in acute hepatitis B virus infection, indicating that the defect in the hepatic interferon-α synthesis is at the level of gene activation. Furthermore, using double immunohistochemical staining, the number of hepatocytes containing HBcAg correlated inversely with the proportion of neighboring sinusoidal cells expressing interferon-α These data support previous observations that interferon-α production is reduced in chronic hepatitis B virus infection and are consistent with the view that this cytokine is important in the clearance of the virus. (HEPATOLOGY 1991;13:1029–1034.)
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