Paez E, Esteban M
J Virol. 1985 Oct;56(1):75-84. doi: 10.1128/JVI.56.1.75-84.1985.
In this report we have shown that Friend erythroleukemia cells persistently infected with vaccinia virus maintain the persistent infection even after 1 year of continuous interferon (IFN) treatment. The persistently infected cultures were responsive to IFN as determined by their ability to induce 2-5A synthetase, to increase the intracellular levels of 2-5A, and to cause rRNA cleavage. While large deletions at the left terminus of vaccinia DNA occurred readily in the virus population from untreated cells, IFN completely suppressed the generation of these spontaneous deletions. Removal of IFN from these cultures led to the appearance of similar deletions at the left terminus of the viral genome. The regions deleted contain more than half of the left-end inverted terminal repetition of the vaccinia genome. These findings show that IFN alters specific events associated with the generation of vaccinia DNA deletions.
在本报告中,我们已经表明,持续感染痘苗病毒的弗氏红白血病细胞即使在连续干扰素(IFN)治疗1年后仍维持持续感染。通过其诱导2-5A合成酶的能力、增加细胞内2-5A水平以及导致rRNA切割的能力来确定,持续感染的培养物对IFN有反应。虽然在未处理细胞的病毒群体中,痘苗病毒DNA左端的大片段缺失很容易出现,但IFN完全抑制了这些自发缺失的产生。从这些培养物中去除IFN会导致病毒基因组左端出现类似的缺失。缺失的区域包含痘苗病毒基因组左端反向末端重复序列的一半以上。这些发现表明,IFN改变了与痘苗病毒DNA缺失产生相关的特定事件。