Sellins K S, Cohen J J
Department of Microbiology and Immunology, University of Colorado School of Medicine, Denver 80262.
J Virol. 1989 Feb;63(2):572-8. doi: 10.1128/JVI.63.2.572-578.1989.
Target cell DNA damage is an early event in cytotoxic T-lymphocyte (CTL)-mediated killing. It has been hypothesized that this DNA damage may serve as one mechanism of destroying viral genetic material inside infected cells. We directly examined the fate of viral DNA in target cells during CTL-mediated lysis. Polyomavirus DNA in transfected murine P815 mastocytoma targets was digested along with cellular DNA into oligonucleosome-sized fragments, although intact forms, possibly virion-associated DNA, were also present. In infected BALB/3T3 murine fibroblasts, which normally undergo single-stranded nicks when killed by CTL, polyomavirus DNA was converted to relaxed forms in the presence of CTL. These results suggest that the fate of the viral DNA depends on the stage of the viral life cycle and corresponds to the fate of the host cell DNA. Cleavage of the viral genome prior to assembly may thus be an important mechanism in specific antiviral immunity.
靶细胞DNA损伤是细胞毒性T淋巴细胞（CTL）介导杀伤过程中的早期事件。据推测，这种DNA损伤可能是破坏受感染细胞内病毒遗传物质的一种机制。我们直接检测了CTL介导裂解过程中靶细胞内病毒DNA的命运。转染的小鼠P815肥大细胞瘤靶细胞中的多瘤病毒DNA与细胞DNA一起被消化成寡核小体大小的片段，不过也存在完整形式，可能是与病毒体相关的DNA。在感染的BALB/3T3小鼠成纤维细胞中，当被CTL杀伤时通常会发生单链切口，在CTL存在的情况下，多瘤病毒DNA会转化为松弛形式。这些结果表明，病毒DNA的命运取决于病毒生命周期的阶段，并且与宿主细胞DNA的命运相对应。因此，在装配之前切割病毒基因组可能是特异性抗病毒免疫中的一种重要机制。
