Abstract
Expression of the viral oncogenes E6 and E7, and telomerase, was investigated, using a cell line from a mild dysplastic vaginal lesion containing human papillomavirus (HPV) type 33. During passaging of the cells, there was a change towards a cancer phenotype, and a shift from episomal to integrated HPV. Levels of hTERT (catalytic subunit of telomerase) mRNA, and telomerase activity in cells carrying episomal virus seemed constant during passaging. During passaging of cells containing integrated HPV, however, the levels of oncogene mRNA decreased, while hTERT mRNA and telomerase activity increased sharply. Thus, in those cells there is no direct correlation between changes of oncogene and telomerase expression. Conceivably, viral oncogene expression might trigger telomerase up-regulation in an early subpopulation of cells, which during subsequent passaging could be selected for.