Thacore H R, Youngner J S
J Virol. 1975 Aug;16(2):322-9. doi: 10.1128/JVI.16.2.322-329.1975.
An abortive infection of a rabbit cornea cell line (RC-60) by vesicular stomatitis virus (VSV), yielding less than 1 PFU/cell, was converted to a productive infection, yielding 1,900 PFU/cell, when cells were superinfected with vaccinia. Studies on the synthesis of VSV-directed RNA in RC-60 cells suggest that the abortive infection by VSV alone may be due in part to (i) a limited production of 40S virion RNA and (ii) a markedly reduced activity of virion-bound transcriptase activity in RC-60 cells compared to the activity in mouse L cells, a permissive host for VSV. No recognizable VSV structures, except a small amount of viral core structures, were produced by the abortive infection. In contrast, double infection of RC-60 cells with VSV and vaccinia in the presence of hydroxyurea resulted in the production of infective B particles of VSV. Although the function supplied by vaccinia responsible for the productive replication of VSV in double infected RC-60 cells has not been identified, metabolic inhibitor studies indicate that continuous vaccinia-dependent RNA synthesis is required for maximal production of infective VSV. The possibility is considered that vaccinia may supply a product or function required for VSV replication which is ordinarily supplied by the host but which is lacking in RC-60 cells.
水泡性口炎病毒(VSV)对兔角膜细胞系(RC - 60)进行的流产感染,每个细胞产生的蚀斑形成单位(PFU)少于1个,当用痘苗病毒对细胞进行超感染时,这种感染转变为增殖性感染,每个细胞产生1900个PFU。对RC - 60细胞中VSV指导的RNA合成的研究表明,单独由VSV引起的流产感染可能部分归因于:(i)40S病毒粒子RNA的产量有限;(ii)与VSV的允许宿主小鼠L细胞中的活性相比,RC - 60细胞中病毒粒子结合的转录酶活性明显降低。流产感染除了产生少量病毒核心结构外,未产生可识别的VSV结构。相比之下,在羟基脲存在的情况下,用VSV和痘苗病毒对RC - 60细胞进行双重感染,导致产生了VSV的感染性B颗粒。虽然痘苗病毒在双重感染的RC - 60细胞中负责VSV增殖性复制所提供的功能尚未确定,但代谢抑制剂研究表明,持续的依赖痘苗病毒的RNA合成对于感染性VSV的最大产量是必需的。有人认为,痘苗病毒可能提供了VSV复制所需的一种产物或功能,这种产物或功能通常由宿主提供,但RC - 60细胞中缺乏。