Watanabe S, Yoshiike K, Nozawa A, Yuasa Y, Uchida S
J Virol. 1979 Dec;32(3):934-42. doi: 10.1128/JVI.32.3.934-942.1979.
A plaque morphology mutant (pm-522) of human papovavirus BK, which was rescued from a human papovavirus BK-induced hamster pineocytoma, was characterized and compared with a cloned wild-type virus (wt-501). Mutant pm-522 formed turbid plaques and grew more slowly than wt-501 in human embryonic kidney (HEK) cells. The immunofluorescence assay revealed that more HEK cells underwent abortive infection with pm-522 than with wt-501. Whereas wt-501 induced brain tumors and osteosarcomas, but no insulinomas, in hamsters, pm-522 induced brain tumors and insulinomas. The DNA of pm-522 was found by electrophoresis and electron microscopy to have a deletion (85 +/- 15 base pairs) and an insertion (40 +/- 10 base pairs) between map coordinates 0.708 and 0.725 from the endonuclease EcoRI cleavage site. These results demonstrate the presence of a viable deletion human papovarivus BK mutant capable of inducing insulinomas in hamsters.
从人乳头瘤病毒BK诱导的仓鼠松果体细胞瘤中拯救出的人乳头瘤病毒BK的一种蚀斑形态突变体(pm - 522),对其进行了特性分析,并与克隆的野生型病毒(wt - 501)进行了比较。突变体pm - 522形成浑浊蚀斑,在人胚肾(HEK)细胞中生长比wt - 501更慢。免疫荧光测定显示,与wt - 501相比,更多的HEK细胞被pm - 522感染后发生流产感染。虽然wt - 501在仓鼠中可诱发脑肿瘤和骨肉瘤,但不诱发胰岛素瘤,而pm - 522可诱发脑肿瘤和胰岛素瘤。通过电泳和电子显微镜发现,pm - 522的DNA在内切酶EcoRI切割位点起,在图谱坐标0.708和0.725之间有一个缺失(85±15个碱基对)和一个插入(40±10个碱基对)。这些结果证明存在一种能够在仓鼠中诱发胰岛素瘤的有活力的缺失型人乳头瘤病毒BK突变体。