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The mechanisms responsible for the human cytomegalovirus (HCMV)-induced increase in cellular oncogene RNAs for c-jun, c-fos, and c-myc in human embryo lung cells (I. Boldogh, S. AbuBakar, and T. Albrecht, Science 247:561-564, 1990) were investigated. Results of transcription assays indicated that the rapid increase in RNA levels for the above-noted oncogenes was controlled at the transcriptional level and was related to enhanced transcription. The maximum rates of transcription for c-jun and c-fos genes occurred at 40 min postinfection, while for the c-myc gene the maximum rate occurred at about 60 min. The magnitude of HCMV-induced activation of these cellular genes was similar to the activation induced by serum. The half-lives of the cellular oncogenes showed similar decay rates after either serum or HCMV activation when measured by dactinomycin chase. The half-life for c-fos or c-jun was about 20 min, and that for c-myc was about 40 min. Furthermore, inhibition of the RNA increase by dactinomycin or by alpha-amanitin suggested that the increase in RNA levels was due to an increase in the transcriptional activity of oncogenes triggered by HCMV.

Transcriptional activation of cellular oncogenes fos, jun, and myc by human cytomegalovirus