Watanabe S, Yoshiike K
J Virol. 1982 Jun;42(3):978-85. doi: 10.1128/JVI.42.3.978-985.1982.
A turbid-plaque-forming mutant (pm522) of human papovavirus BK, which has a small deletion at about 0.7 map unit and grows somewhat more slowly in human cells than does wild-type BK virus, transformed hamster and rat cells in culture much more efficiently than did wild-type virus. Another plaque morphology mutant, pm525, forming turbid plaques larger than those of pm522 also had a high transforming capacity. The similar difference in transforming capability between wild-type and plaque morphology viruses was observed with DNAs extracted from virions. Recombinant viruses were constructed from the wild-type DNA fragment lacking HindIII-C (0.62 to 0.73 map unit) and pm522 HindIII-C (including the origin of replication) by the molecular cloning method. Characterization of the recombinants showed that the change near the origin of DNA replication was responsible both for the altered plaque morphology and for the enhanced transforming capacity of the BK virus mutant.
人乳头瘤病毒BK的一个形成浑浊蚀斑的突变体（pm522），在约0.7个图距单位处有一个小缺失，在人细胞中的生长速度比野生型BK病毒稍慢，但其在培养中转化仓鼠和大鼠细胞的效率比野生型病毒高得多。另一个蚀斑形态突变体pm525，形成的浑浊蚀斑比pm522的大，其转化能力也很强。从病毒粒子中提取的DNA也观察到野生型和蚀斑形态病毒在转化能力上有类似差异。通过分子克隆方法，用缺乏HindIII-C（0.62至0.73个图距单位）的野生型DNA片段和pm522的HindIII-C（包括复制起点）构建了重组病毒。对重组体的特性分析表明，DNA复制起点附近的变化既导致了蚀斑形态的改变，也导致了BK病毒突变体转化能力的增强。
