Yoshiike K, Watanabe S
Gan To Kagaku Ryoho. 1984 Mar;11(3 Pt 2):571-8.
We characterized a plaque-morphology mutant of human papovavirus BK (pm-522), which can transform rat 3Y1 cells much more efficiently than a wild type (wt-501) does. Unintegrated pm-522 genomes appeared to be continuously transcribed, to direct synthesis of large T antigen, and to cause abortive transformation of the infected rat cells during the first two-week period before foci of the stably transformed cells develop. Despite the initial transcription and T antigen production, wt-501 genomes ceased being transcribed soon. T antigen, together with a yet unidentified factor from rat cells, may suppress transcription of the wt early genome. The difference in control of early transcription of the free viral genomes in rat cells could account for the difference in transforming capacity between wt-501 and pm-522. Some of the three small deletions clustering in the probable transcriptional control region were found to be responsible for the plaque morphology and high-transforming capacity of pm-522. Comparison of nucleotide sequences between the two viruses indicated that pm-522 was probably generated from wt-501 through deletion followed by two small local duplications in the area containing 68-base-pair repeats characteristic of BK virus.