The intrahepatic accumulation of the c‐myc protooncogene product was observed on immunoflourescence in each of six patients with chronic hepatitis delta virus infection who exhibited the hepatitis D antigen in their livers. The c‐myc product was stained in the same nuclei that contained the hepatitis D antigen. C‐myc was not observed in acute hepatitis D or in cases of chronic hepatitis delta virus infection without expression of the hepatitis D antigen. The protooncogene product was detected in only 1 of 32 viral and nonviral liver disorders unrelated to hepatitis delta virus. To confirm these observations, we transfected HBsAg‐positive (PCL/PRF/5) and HBsAg‐negative (HepG2) transformed liver cell lines with a plasmid containing a hepatitis delta virus cDNA trimer under the control of the SV40 early enhancer/promoter sequences. Whereas baseline c‐myc expression was barely detectable in mock‐transfected PLC/PRF/5 or HepG2 cells, strong c‐myc nuclear fluorescence was observed when these same cells were transfected with the hepatitis D antigen expression vector. Similar results were obtained after infection of HeLa cells with a recombinant vaccinia virus expressing the hepatitis D antigen. Detection of c‐myc mRNA sequences by means of in situ hybridization suggested that the c‐myc product accumulation was not due to increased amounts of its mRNA. The c‐myc protein accumulates selectively in the livers of patients with chronic hepatitis delta virus infection and in the same nuclei that contain the hepatitis D antigen. The expression of c‐myc in hepatitis D antigencontaining cells does not require the presence of hepatitis B virus infection. (Hepatology 1994;20:1109–1114).
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