Ostertag W, Roesler G, Krieg C J, Kind J, Cole T, Crozier T, Gaedicke G, Steinheider G, Kluge N, Dube S
Proc Natl Acad Sci U S A. 1974 Dec;71(12):4980-5. doi: 10.1073/pnas.71.12.4980.
Thymidine kinase positive (TK(+)) N type cell lines that had been transformed by spleen focus-forming virus were established by transformation with NB tropic Friend virus complex. Thymidine kinase deficient (TK(-)) cell clones were isolated. Some of these cell clones release 1000- to 100,000-fold reduced amounts of Friend virus complex as compared to the TK(+) parental cell clone. TK(-) clones were grown in medium without BrdUrd. Some of these TK(-) clones can be induced to release endogenous helper virus and transforming spleen focus-forming virus on reexposure to 10(-6)-10(-4) M BrdUrd. The induced Friend virus complex is of N host range as expected with induced endogenous virus in N-type cells. Before the induction of the endogenous virus spleen focus-forming virus complex, an induction of thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.75) activity is observed. The latter is possibly a prerequisite for the induction of endogenous virus in TK(-) cells. Induction of thymidine kinase activity and of endogenous virus is transient and always correlated. The role of BrdUrd and another thymidine analogue, azidothymidine, in interfering with C-type virus release in virus positive cells is discussed. Azidothymidine is unable to induce endogenous virus. Induction of endogenous virus by BrdUrd and inhibition of virus release in virus positive cells is apparently not caused by the same mechanism.
通过用嗜N型弗氏病毒复合物转化，建立了经脾集落形成病毒转化的胸苷激酶阳性（TK(+)）N型细胞系。分离出胸苷激酶缺陷（TK(-)）细胞克隆。与TK(+)亲代细胞克隆相比，其中一些细胞克隆释放的弗氏病毒复合物量减少了1000至100000倍。TK(-)克隆在不含溴脱氧尿苷（BrdUrd）的培养基中生长。其中一些TK(-)克隆在重新暴露于10(-6)-10(-4)M BrdUrd时可被诱导释放内源性辅助病毒和转化性脾集落形成病毒。诱导产生的弗氏病毒复合物具有N宿主范围，这与N型细胞中诱导产生的内源性病毒预期一致。在内源性病毒脾集落形成病毒复合物诱导之前，观察到胸苷激酶（ATP:胸苷5'-磷酸转移酶，EC 2.7.1.75）活性的诱导。后者可能是TK(-)细胞中内源性病毒诱导的先决条件。胸苷激酶活性和内源性病毒的诱导是短暂的且始终相关。讨论了BrdUrd和另一种胸苷类似物叠氮胸苷在干扰病毒阳性细胞中C型病毒释放方面的作用。叠氮胸苷不能诱导内源性病毒。BrdUrd诱导内源性病毒以及抑制病毒阳性细胞中病毒释放显然不是由相同机制引起的。
