Paez E, Esteban M
Department of Biochemistry, State University of New York, Brooklyn 11203.
Virology. 1988 Mar;163(1):145-54. doi: 10.1016/0042-6822(88)90241-3.
The stability of the large vaccinia virus genome (122 MDa) has been studied in long-term cultures of persistently infected Friend erythroleukemia (FEL) cells. Deletions of about 8 MDa at the left terminus of vaccinia DNA are generated at early passages, and are maintained even after 2 years of continuous cell passages. The generation of deletions is followed by a stable accumulation of tandem repeats up to 6 MDa at the left end and up to 2 MDa at the right end of vaccinia DNA. Neither translocations nor rearrangements of DNA are observed during persistent infection. A recombinational mechanism within the tandem repeats or a mechanism similar to that described for adenovirus might explain the reiteration of tandem repeats at both ends. Significantly, in persistently infected cultures continuously treated with interferon (IFN) both the deletion and the large accumulation of tandem repeats were completely blocked. We suggest that reiteration of tandem repeats at the termini of vaccinia DNA might provide signals for more efficient virus multiplication in FEL cells.
在持续感染的弗氏红白血病（FEL）细胞的长期培养中，研究了大型痘苗病毒基因组（122 MDa）的稳定性。在早期传代时，痘苗病毒DNA左端会产生约8 MDa的缺失，并且即使在连续传代2年后仍会保留。缺失产生后，痘苗病毒DNA左端会稳定积累高达6 MDa的串联重复序列，右端则高达2 MDa。在持续感染期间未观察到DNA的易位或重排。串联重复序列内的重组机制或类似于腺病毒所描述的机制可能解释了两端串联重复序列的重复。值得注意的是，在持续用干扰素（IFN）处理的感染培养物中，缺失和串联重复序列的大量积累均被完全阻断。我们认为，痘苗病毒DNA末端串联重复序列的重复可能为FEL细胞中更有效的病毒增殖提供信号。
