Copyright C) 1991, American Society for Microbiology NOTES Transcriptional Activation of Cellular Oncogenes fos, jun, and myc

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 ofHCMV-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 a-amanitin suggested that the increase in RNA levels was due to an increase in the transcriptional activity of oncogenes triggered by HCMV. Human cytomegalovirus (HCMV) infections stimulate cel-lular DNA synthesis and cell proliferation (5, 8, 9), and this activation process appears to be related to the pathogenesis of HCMV infections (4). Consistent with these findings