Klimkait T, Doerfler W
J Virol. 1985 Aug;55(2):466-74. doi: 10.1128/JVI.55.2.466-474.1985.
Human adenovirus type 12 (Ad12) cannot replicate in hamster cells. There is a complete block of viral DNA replication and of the expression of late viral genes. Early viral functions are expressed. In contrast, hamster cells are permissive for human adenovirus type 2 (Ad2). Some of the Ad12-specific functions are insufficient to support viral replication in hamster cells, or else cellular functions are missing or inhibitory for Ad12 replication. It was shown that the block in the replication and late expression of the Ad12 genome in hamster cells could, at least in part, be complemented by Ad2 and adenovirus type 5 (Ad5) functions. When hamster cells were coinfected with Ad2 (or Ad5) and Ad12, both Ad2 (Ad5) and Ad12 DNA replicated. Ad2 (Ad5) virions were produced in double-infected hamster cells. The assembly of intact Ad12 virions was not detectable by the techniques used here. The analysis was further refined by Ad12 superinfecting Ad2- or Ad5-transformed cells which carried in an integrated form defined fragments of the Ad2 or Ad5 genome. Persistence and continued expression of the left terminus of the Ad2 or Ad5 DNA in these cells has been documented and helped to support replication and late expression of Ad12 DNA. It remains to be determined which of the E1 functions of Ad2 or Ad5 were responsible for the helper effect. Investigations on the biochemical mechanism of this complementation will entail studies on very complex viral and possibly cellular functions involved in the control of viral gene expression.
人腺病毒12型(Ad12)无法在仓鼠细胞中复制。病毒DNA复制以及晚期病毒基因的表达完全受阻。早期病毒功能则可表达。相比之下,仓鼠细胞对人腺病毒2型(Ad2)具有感染性。Ad12的某些特异性功能不足以支持其在仓鼠细胞中的复制,或者是细胞功能缺失或对Ad12复制具有抑制作用。研究表明,仓鼠细胞中Ad12基因组复制和晚期表达的阻滞至少部分可由Ad2和腺病毒5型(Ad5)的功能互补。当仓鼠细胞同时感染Ad2(或Ad5)和Ad12时,Ad2(Ad5)和Ad12的DNA都会复制。在双重感染的仓鼠细胞中会产生Ad2(Ad5)病毒粒子。此处使用的技术无法检测到完整Ad12病毒粒子的组装。通过Ad12超感染携带整合形式的Ad2或Ad5基因组特定片段的Ad2或Ad5转化细胞,分析得到了进一步完善。这些细胞中Ad2或Ad5 DNA左末端的持续存在和持续表达已得到证实,并有助于支持Ad12 DNA的复制和晚期表达。尚待确定Ad2或Ad5的哪些E1功能导致了这种辅助作用。对这种互补作用生化机制的研究将需要对病毒基因表达调控中涉及的非常复杂的病毒及可能的细胞功能进行研究。