Brown A, Consigli R A, Zabielski J, Weil R
J Virol. 1974 Oct;14(4):840-5. doi: 10.1128/JVI.14.4.840-845.1974.
Polyoma virus was inactivated by treatment with beta-propiolactone. T-antigen production, polyoma-RNA synthesis, induction of host DNA synthesis (measured by incorporation of labeled thymidine into the cell culture), and in vitro transforming ability were inactivated to a similar degree by various beta-propiolactone concentrations (0.25% beta-propiolactone reduced these functions approximately 96%), whereas plaque-forming ability and the ability of the virus to replicate its DNA and to synthesize capsid antigen were inactivated by a given concentration of beta-propiolactone to a much greater degree (0.25% beta-propiolactone led to a reduction of plaque-forming ability of over 8 logs). The significance of these data and their relationship to previously published experiments are discussed.
多瘤病毒经β-丙内酯处理后失活。不同浓度的β-丙内酯(0.25%的β-丙内酯使这些功能降低约96%)对T抗原产生、多瘤病毒RNA合成、宿主DNA合成的诱导(通过将标记的胸苷掺入细胞培养物中来测量)以及体外转化能力的失活程度相似,而空斑形成能力以及病毒复制其DNA和合成衣壳抗原的能力在给定浓度的β-丙内酯作用下失活程度要大得多(0.25%的β-丙内酯导致空斑形成能力降低超过8个对数级)。讨论了这些数据的意义及其与先前发表的实验的关系。