Pothier P, Dru A, Beaud G
J Gen Virol. 1981 Jul;55(Pt 1):87-94. doi: 10.1099/0022-1317-55-1-87.
The step sensitive to DRB (5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole) in vaccinia virus replication has been investigated. Ninety microM-DRB extensively inhibited the yield of vaccinia virus after infection of Ehrlich ascites tumour cells. DRB did not inhibit cytoplasmic vaccinia DNA replication. Cytoplasmic viral RNA synthesis (both early and late) was also apparently unaffected and the virus RNAs thus synthesized were normal sized. The expression of early, intermediate and late proteins was not detectably impaired by DRB in vaccinia virus-infected cells. DRB inhibited vaccinia virus replication at the assembly stage since most of the virus DNA remained in a DNase-sensitive form in the infected cells and the virus was therefore not normally coated with virus proteins.
对痘苗病毒复制中对DRB（5,6 - 二氯 - 1 - β - D - 呋喃核糖基苯并咪唑）敏感的步骤进行了研究。90微摩尔的DRB在感染艾氏腹水瘤细胞后广泛抑制痘苗病毒的产量。DRB不抑制细胞质中的痘苗病毒DNA复制。细胞质病毒RNA合成（早期和晚期）也明显未受影响，并且如此合成的病毒RNA大小正常。在痘苗病毒感染的细胞中，DRB未可检测到地损害早期、中期和晚期蛋白质的表达。DRB在组装阶段抑制痘苗病毒复制，因为在感染细胞中大部分病毒DNA保持对DNase敏感的形式，因此病毒通常没有被病毒蛋白包裹。
