Keller F, Drillien R, Kirn A
Infect Immun. 1979 Dec;26(3):841-7. doi: 10.1128/iai.26.3.841-847.1979.
Studies of the in vivo multiplication of an attenuated temperature-sensitive strain of vaccinia virus (ts2) indicated that temperature sensitivity alone could not account for the attenuation. Immunodepressive treatment of intracerebrally inoculated mice had a dramatic stimulatory effect on the multiplication of the attenuated strain and suggested that establishment of ts2 infection in the mice was hindered by host defense mechanisms mediated by cellular elements. Experiments carried out in vitro with the 51Cr release assay showed that cells infected with the ts2 mutant represented more susceptible targets to the cytotoxic action of immune spleen cells than cells infected with the parent vaccinia strain. Moreover, it appeared that ts2 replication, compared with wild-type replication in vitro, was more inhibited by the immune spleen cells. Although this work did not evaluate the role of specifically sensitized lymphocytes within the lesions, indirect evidence suggests that lymphocytes could cause a more effective halt in ts2 virus multiplication than in wild-type multiplication.
对痘苗病毒减毒温度敏感株(ts2)体内增殖的研究表明,仅温度敏感性不能解释其减毒现象。对脑内接种小鼠进行免疫抑制治疗对该减毒株的增殖有显著的刺激作用,这表明ts2在小鼠体内的感染建立受到细胞成分介导的宿主防御机制的阻碍。用51Cr释放试验进行的体外实验表明,与感染亲本痘苗病毒株的细胞相比,感染ts2突变体的细胞是免疫脾细胞细胞毒性作用更敏感的靶标。此外,与体外野生型复制相比,ts2复制似乎更受免疫脾细胞的抑制。尽管这项工作没有评估损伤部位特异性致敏淋巴细胞的作用,但间接证据表明,淋巴细胞对ts2病毒增殖的阻止作用可能比对野生型增殖的阻止作用更有效。