Abstract
One of the outcomes of persistent viral infection is carcinogenesis, often characterized by viral genome or genome fragments integrated into cellular DNA at one or more points (667). The strong association of HBV with primary hepatocellular carcinoma (PHC) (89, 90, 94, 95, 536, 537, 668), combined with the apparent findings of greater than unit length HBV DNA association with Dane particles (607, 641), suggest that these longer species may be derived from integrated virus DNA which carried additional host material with it upon excision (639). The presence and state of HBV DNA in tumor tissues was subsequently examined by accelerated annealing of a 32P-labeled HBV DNA probe in solution and by agarose gel electrophoresis (669, Table 15). Two tumors from different patients had detectable viral DNA at levels of approximately 1–2 genomes per cell, a third tumor from another patient resulted in levels less than 0.1 genome per cell, while a fourth isolate from another source contained no detectable viral DNA. Although the cellular DNA in the autopsy tumors was extensively degraded, preventing assessment of any integrated sequences, full-length HBV DNA was detected in some cases, suggesting its protection inside Dane particle cores.
Published Version
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